A 35 year-old Caucasian male presents with persistent swelling of both legs associated with dark colored urine for two months. He went to an emergency room 2 months ago for these complaints and was told that he has some protein and blood in the urine. He was treated with 3 days of levofloxacin. There is no other past medical history. No history of skin rash or joint swelling. On examination the blood pressure was 130/85 mm Hg and there was bilateral 1+ pedal edema. Rest of the physical examination was normal. Urine analysis showed 3+ proteinuria, 10-15 RBCs per high-power field, and occasional RBC cast. The BUN was 10 mg/dL, serum creatinine was 0.9 mg/dL. Antistreptolysin was negative, C3 level is decreased and C4 level is normal. Antinuclear antibodies, ANCA, hepatitis B and C serology were negative. 24-hour urine collection showed 2 g proteinuria and a kidney biopsy was performed. On light microscopy, kidney biopsy showed increase in the mesangial matrix and cellularity and glomerular basement membrane appeared irregularly thickened. Silver stain revealed duplication of glomerular basement membrane in multiple glomeruli. Immunofluorescence showed positive staining for C3, but negative for IgG, IgM and IgA. Electron microscopy revealed electron-dense deposits in the mesangium and sub-endothelial area. 

What is the most likely diagnosis?

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Created On: 09/12/2017
Last Modified: 03/07/2021

A 35 year-old Caucasian male presents with persistent swelling of both legs associated with dark colored urine for two months. He went to an emergency room 2 months ago for these complaints and was told that he has some protein and blood in the urine. He was treated with 3 days of levofloxacin. There is no other past medical history. No history of skin rash or joint swelling. On examination the blood pressure was 130/85 mm Hg and there was bilateral 1+ pedal edema. Rest of the physical examination was normal. Urine analysis showed 3+ proteinuria, 10-15 RBCs per high-power field, and occasional RBC cast. The BUN was 10 mg/dL, serum creatinine was 0.9 mg/dL. Antistreptolysin was negative, C3 level is decreased and C4 level is normal. Antinuclear antibodies, ANCA, hepatitis B and C serology were negative. 24-hour urine collection showed 2 g proteinuria and a kidney biopsy was performed. On light microscopy, kidney biopsy showed increase in the mesangial matrix and cellularity and glomerular basement membrane appeared irregularly thickened. Silver stain revealed duplication of glomerular basement membrane in multiple glomeruli. Immunofluorescence showed positive staining for C3, but negative for IgG, IgM and IgA. Electron microscopy revealed electron-dense deposits in the mesangium and sub-endothelial area. 

What is the most likely diagnosis?

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Created On: 09/12/2017
Last Modified: 03/07/2021

A 25 year-old male comes to the physician complaining of flank pain and hematuria.  He says the pain is constant and dull. There is no frequency, urgency or dysuria.  He has a history of mental retardation and seizures. On physical exam his blood pressure is 140/90 mm Hg, and his pulse is 80 bpm. He has multiple yellow papules across his nose and cheeks and numerous areas of blanched skin spots on his face. A 2-3 cm hypopigmented macule is noted on the right arm. CT scan of the head was done as patient presented with seizures. CT head was reported normal. CT scan of the abdomen shows bilateral hypodense fat containing renal masses and cysts. 

What is the MOST likely diagnosis associated with these findings?

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Created On: 09/13/2017
Last Modified: 12/30/2017

A 25 year-old male comes to the physician complaining of flank pain and hematuria.  He says the pain is constant and dull. There is no frequency, urgency or dysuria.  He has a history of mental retardation and seizures. On physical exam his blood pressure is 140/90 mm Hg, and his pulse is 80 bpm. He has multiple yellow papules across his nose and cheeks and numerous areas of blanched skin spots on his face. A 2-3 cm hypopigmented macule is noted on the right arm. CT scan of the head was done as patient presented with seizures. CT head was reported normal. CT scan of the abdomen shows bilateral hypodense fat containing renal masses and cysts. 

What is the MOST likely diagnosis associated with these findings?

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Created On: 09/13/2017
Last Modified: 12/30/2017

A 68 year-old African American male with known history of diabetes mellitus,  hyperlipidemia, CVD, and GERD presents to the ER with chest pain and shortness of breath. Patient says the pain is a crushing pain and radiating to his left arm. It woke him from sleep 30 minutes ago. He took his antacids and 4 tablets of nitroglycerin, and the pain got better. His current medications include low dose aspirin, metoprolol, glyburide, pioglitazone, lisinopril, simvastatin, and omeprazole. He recently suffered an upper respiratory infection for which he was given Levofloxacin. Vitals show: BP 160/95 mm Hg, T 98.1, and HR 110. He has no edema legs and no jugular venous distention. EKG shows LVH by voltage criteria with isoelectric ST segment. Serial troponin levels are normal. A stress test showed evidence of stress inducible ischemia in the anterior leads. He is scheduled for cardiac catheterization the next day. Laboratory results are as follows:

Serum Chemistry:

Na   143 mEq/L

K   3.5 mEq/L

Cl   101 mEq/L

HCO3  22 mEq/L

BUN   35 mg/dL

Cr   3.0 mg/dL

Glucose  110 mg/dL 

What would you do to PROTECT the kidneys before doing the cardiac catheterization?

• Low fractional excretion of sodium (FeNa) below 1%.
• Iodinated contrast agents test false positive for protein and hence proteinuria gets overestimated
• It is reversible most of the time
• UA may show muddy brown granular casts, tubular epithelial cell casts and numerous tubular epithelial casts.

• Chronic kidney disease
• Diabetes mellitus
• Congestive heart failure
• Myeloma kidney
• Hypotension

Copyright © ABIM Exam World
Created On: 09/14/2017
Last Modified: 08/06/2018

A 68 year-old African American male with known history of diabetes mellitus,  hyperlipidemia, CVD, and GERD presents to the ER with chest pain and shortness of breath. Patient says the pain is a crushing pain and radiating to his left arm. It woke him from sleep 30 minutes ago. He took his antacids and 4 tablets of nitroglycerin, and the pain got better. His current medications include low dose aspirin, metoprolol, glyburide, pioglitazone, lisinopril, simvastatin, and omeprazole. He recently suffered an upper respiratory infection for which he was given Levofloxacin. Vitals show: BP 160/95 mm Hg, T 98.1, and HR 110. He has no edema legs and no jugular venous distention. EKG shows LVH by voltage criteria with isoelectric ST segment. Serial troponin levels are normal. A stress test showed evidence of stress inducible ischemia in the anterior leads. He is scheduled for cardiac catheterization the next day. Laboratory results are as follows:

Serum Chemistry:

Na   143 mEq/L

K   3.5 mEq/L

Cl   101 mEq/L

HCO3  22 mEq/L

BUN   35 mg/dL

Cr   3.0 mg/dL

Glucose  110 mg/dL 

What would you do to PROTECT the kidneys before doing the cardiac catheterization?

• Low fractional excretion of sodium (FeNa) below 1%.
• Iodinated contrast agents test false positive for protein and hence proteinuria gets overestimated
• It is reversible most of the time
• UA may show muddy brown granular casts, tubular epithelial cell casts and numerous tubular epithelial casts.

• Chronic kidney disease
• Diabetes mellitus
• Congestive heart failure
• Myeloma kidney
• Hypotension

Copyright © ABIM Exam World
Created On: 09/14/2017
Last Modified: 08/06/2018

A 56 year-old male was brought to the emergency room with drowsiness and lethargy. He has been experiencing these for the last 2 days. He complains of a recent history of anorexia, nausea, and vomiting, He has diabetes mellitus and is on glimepiride 1 mg daily for the last 4 years. One week ago he had decreased vision with redness in his right eye. He was treated by his ophthalmologist with drops which seem to have resolved the problem. He currently takes cholecalciferol weekly for osteoporosis. On physical examination his pulse is 80/min, blood pressure is 140/90 mm Hg, respiratory rate is 20/min, and temperature is 97.7 F. The patient appears drowsy but shows no focal neurological deficits. Review of systems is otherwise unremarkable. Urinalysis is positive for glucose and negative for proteinuria, WBCs and RBC casts. A 24 hour urinary protein collection is significant for proteinuria of 3.5 g/day. Further labs reveal:

Hemoglobin  8 gm%

Hct    24%

MCV   85

WBC   7800/ml

PMN   80%

Lymphocytes  20%

ESR   80 mm/hr

Na    145 mEq/L

BUN   80 mg/dL

Cr    1.8 mg/dL

CL    115 mEq/L

HCO3   25 mEq/L

Uric acid   5.8 mg/dL

Ca    14 mg/dl

PO4    2.8 mg/dL

Total Protein  7.8 gm/dL

Albumin   3.5 mg/dL.

Vitamin D  40 ng/ml

PTH   10 pg/ml

Which of the following is most likely the cause of his hypercalcemia?

• Advanced Age

• Backache and Bone pain

• Anemia

• High ESR

• Urine protein negative by dipstick and positive by other tests is characteristic of light chain proteinuria.

• High Total protein

• Low anion gap

• Hypercalcemia and hyperuricemia favors the diagnosis of multiple myeloma.

Copyright © ABIM Exam World
Created On: 09/20/2017
Last Modified: 08/06/2018

A 56 year-old male was brought to the emergency room with drowsiness and lethargy. He has been experiencing these for the last 2 days. He complains of a recent history of anorexia, nausea, and vomiting, He has diabetes mellitus and is on glimepiride 1 mg daily for the last 4 years. One week ago he had decreased vision with redness in his right eye. He was treated by his ophthalmologist with drops which seem to have resolved the problem. He currently takes cholecalciferol weekly for osteoporosis. On physical examination his pulse is 80/min, blood pressure is 140/90 mm Hg, respiratory rate is 20/min, and temperature is 97.7 F. The patient appears drowsy but shows no focal neurological deficits. Review of systems is otherwise unremarkable. Urinalysis is positive for glucose and negative for proteinuria, WBCs and RBC casts. A 24 hour urinary protein collection is significant for proteinuria of 3.5 g/day. Further labs reveal:

Hemoglobin  8 gm%

Hct    24%

MCV   85

WBC   7800/ml

PMN   80%

Lymphocytes  20%

ESR   80 mm/hr

Na    145 mEq/L

BUN   80 mg/dL

Cr    1.8 mg/dL

CL    115 mEq/L

HCO3   25 mEq/L

Uric acid   5.8 mg/dL

Ca    14 mg/dl

PO4    2.8 mg/dL

Total Protein  7.8 gm/dL

Albumin   3.5 mg/dL.

Vitamin D  40 ng/ml

PTH   10 pg/ml

Which of the following is most likely the cause of his hypercalcemia?

• Advanced Age

• Backache and Bone pain

• Anemia

• High ESR

• Urine protein negative by dipstick and positive by other tests is characteristic of light chain proteinuria.

• High Total protein

• Low anion gap

• Hypercalcemia and hyperuricemia favors the diagnosis of multiple myeloma.

Copyright © ABIM Exam World
Created On: 09/20/2017
Last Modified: 08/06/2018

A 25 year-old female is referred by her primary care provider for evaluation of hypertension and hypokalemia. The primary care provider has already started her on oral potassium, despite therapy her Potassium being 2.8 meq/L. Her blood pressure despite treatment with amlodipine and Lisinopril 154/96 mm of Hg. There is no renal bruit. Systemic and fundus examinations are normal. Her mother was also diagnosed with hypertension at an early age. Her brother died of a cerebrovascular accident 2 years ago. Laboratory findings are as follows:

Na   140 

Potassium 2.8 

Chloride   100 

HCO3    26

BUN   15 

Creatinine  0.8 

Glucose    110

TSH and Cortisol are normal

ACTH    elevated

Renin   0.7 (Low)

Aldosterone  48 (elevated)

Urinalysis:

Sodium   240 mEq/D

Potassium  98 mEq/D

Urinary 18-OH Cortisol and 18-oxocortisol are elevated.

The most appropriate treatment for this patient is:

Copyright © ABIM Exam World
Created On: 09/20/2017
Last Modified: 08/06/2018

A 25 year-old female is referred by her primary care provider for evaluation of hypertension and hypokalemia. The primary care provider has already started her on oral potassium, despite therapy her Potassium being 2.8 meq/L. Her blood pressure despite treatment with amlodipine and Lisinopril 154/96 mm of Hg. There is no renal bruit. Systemic and fundus examinations are normal. Her mother was also diagnosed with hypertension at an early age. Her brother died of a cerebrovascular accident 2 years ago. Laboratory findings are as follows:

Na   140 

Potassium 2.8 

Chloride   100 

HCO3    26

BUN   15 

Creatinine  0.8 

Glucose    110

TSH and Cortisol are normal

ACTH    elevated

Renin   0.7 (Low)

Aldosterone  48 (elevated)

Urinalysis:

Sodium   240 mEq/D

Potassium  98 mEq/D

Urinary 18-OH Cortisol and 18-oxocortisol are elevated.

The most appropriate treatment for this patient is:

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Created On: 09/20/2017
Last Modified: 08/06/2018

A 60 year-old with recently diagnosed colon cancer and diabetes presents with bilateral pedal edema, BP is 120/80 mm Hg, Urinalysis showed  4+ protein, no RBCs or WBCs, and 8-10 Hyaline casts. His BUN is 20, Creatinine is 1 mg/dL, and albumin is 2 grams/dL. 24 hour urine collection showed 10 grams protein. The patient undergoes kidney biopsy. The EM is shown below :

What is the most likely diagnosis?

The correct answer is E

Membranous Nephropathy.

The Electron microscopy shows subepithelial electron dense deposit as classically seen in membranous nephropathy. If in the question there is a suggestion of colon, breast, or lung cancer, then the glomerulopathy is usually membranous. After that look for other findings on histopathology which will confirm the diagnosis. Subepithelial electron dense deposits.

Explanation:

BOARD POINT - FAMILIARIZE YOURSELF WITH THESE ASSOCIATIONS :

1. Solid cancers (colon, breast, lung, renal) plus proteinuria = Membranous nephropathy

2. Hodgkins lymphoma plus proteinuria = Minimal change disease

3. HIV plus proteinuria = Focal segment glomerulosclerosis FSGS

4. Pamidronate plus protenuria = FSGS (rare)

5. Myeloma, no albuminuria on dipstix, but proteinuria on protein/creatinine ratio or 24 hrs urine: Light chain nephropathy

6. Myeloma with non specific proteinuria (on dipstix, urine protein/creatinine ratio and 24 hrs urine): Light chain nephropathy or amyloidosis.

BOARD POINT - FAMILIARIZE YOURSELF WITH THESE HISTOPATHOLOGY ASSOCIATIONS FOR VARIOUS GLOMERULAR DISEASES

Copyright © ABIM Exam World
Created On: 09/20/2017
Last Modified: 08/29/2018

A 60 year-old with recently diagnosed colon cancer and diabetes presents with bilateral pedal edema, BP is 120/80 mm Hg, Urinalysis showed  4+ protein, no RBCs or WBCs, and 8-10 Hyaline casts. His BUN is 20, Creatinine is 1 mg/dL, and albumin is 2 grams/dL. 24 hour urine collection showed 10 grams protein. The patient undergoes kidney biopsy. The EM is shown below :

What is the most likely diagnosis?

The correct answer is E

Membranous Nephropathy.

The Electron microscopy shows subepithelial electron dense deposit as classically seen in membranous nephropathy. If in the question there is a suggestion of colon, breast, or lung cancer, then the glomerulopathy is usually membranous. After that look for other findings on histopathology which will confirm the diagnosis. Subepithelial electron dense deposits.

Explanation:

BOARD POINT - FAMILIARIZE YOURSELF WITH THESE ASSOCIATIONS :

1. Solid cancers (colon, breast, lung, renal) plus proteinuria = Membranous nephropathy

2. Hodgkins lymphoma plus proteinuria = Minimal change disease

3. HIV plus proteinuria = Focal segment glomerulosclerosis FSGS

4. Pamidronate plus protenuria = FSGS (rare)

5. Myeloma, no albuminuria on dipstix, but proteinuria on protein/creatinine ratio or 24 hrs urine: Light chain nephropathy

6. Myeloma with non specific proteinuria (on dipstix, urine protein/creatinine ratio and 24 hrs urine): Light chain nephropathy or amyloidosis.

BOARD POINT - FAMILIARIZE YOURSELF WITH THESE HISTOPATHOLOGY ASSOCIATIONS FOR VARIOUS GLOMERULAR DISEASES

Copyright © ABIM Exam World
Created On: 09/20/2017
Last Modified: 08/29/2018

A 36 year-old female was diagnosed as having membranous nephropathy secondary to SLE. Her 24 hour protein excretion was 7.5 gms/day. Her serum creatinine was 0.9mg/dl. She was started on 500 mg of cyclophosphamide IV every 15 days (Euro-Lupus) and prednisolone 1 mg/kg orally per day. After 3 months of therapy, she presented with decreased urine output, puffiness of face, and oedema feet. On physical examination, her temperature is 37 C, blood pressure is 160/100 mm Hg, pulse is 90/min, and respiration rate is 20/min. She is anemic and there is puffiness of the face and oedema of the feet. On systemic examination air entry was decreased in the bases of both the lung fields and heart sounds are distant and feeble. Chest X-Ray reveals bilateral pleural effusions. Echocardiogram reveals mild to moderate pericardial effusion. Laboratory examination is as follows: 

Hemoglobin   10.0 g/dL

Hematocrit   34%

Platelet Count   150,000 mm3

WBC    8,000 mm3

Differential count P  80% L 12% E 6% M 2%

ESR    50.8 mm/h

Urinalysis: 

Protein  1450 mg/24 h

Glucose  None

RBCs  70-80/HPF dysmorphic

WBCs  5-8/HPF

Leukocyte Esterase Negative

Nitrites  Negative

 BUN   35 mg/dL

Creatinine  3.9 mg/dL

Sodium   140 mEq/L

Potassium  5.2 mEq/L

Bicarbonate  15.5 mEq/L

Calcium   9.2 mEq/L

Phosphorus  5.6 mg/dL

Glucose   100 mg/dL

Uric Acid   5.3 mg/dL

C3 & C4 decreased 

ANA   positive

dsDNA   positive

Repeat biopsy shows:

Which of the following is the most appropriate therapy for her current condition?

Copyright © ABIM Exam World
Created On: 09/20/2017
Last Modified: 08/06/2018

A 36 year-old female was diagnosed as having membranous nephropathy secondary to SLE. Her 24 hour protein excretion was 7.5 gms/day. Her serum creatinine was 0.9mg/dl. She was started on 500 mg of cyclophosphamide IV every 15 days (Euro-Lupus) and prednisolone 1 mg/kg orally per day. After 3 months of therapy, she presented with decreased urine output, puffiness of face, and oedema feet. On physical examination, her temperature is 37 C, blood pressure is 160/100 mm Hg, pulse is 90/min, and respiration rate is 20/min. She is anemic and there is puffiness of the face and oedema of the feet. On systemic examination air entry was decreased in the bases of both the lung fields and heart sounds are distant and feeble. Chest X-Ray reveals bilateral pleural effusions. Echocardiogram reveals mild to moderate pericardial effusion. Laboratory examination is as follows: 

Hemoglobin   10.0 g/dL

Hematocrit   34%

Platelet Count   150,000 mm3

WBC    8,000 mm3

Differential count P  80% L 12% E 6% M 2%

ESR    50.8 mm/h

Urinalysis: 

Protein  1450 mg/24 h

Glucose  None

RBCs  70-80/HPF dysmorphic

WBCs  5-8/HPF

Leukocyte Esterase Negative

Nitrites  Negative

 BUN   35 mg/dL

Creatinine  3.9 mg/dL

Sodium   140 mEq/L

Potassium  5.2 mEq/L

Bicarbonate  15.5 mEq/L

Calcium   9.2 mEq/L

Phosphorus  5.6 mg/dL

Glucose   100 mg/dL

Uric Acid   5.3 mg/dL

C3 & C4 decreased 

ANA   positive

dsDNA   positive

Repeat biopsy shows:

Which of the following is the most appropriate therapy for her current condition?

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Created On: 09/20/2017
Last Modified: 08/06/2018

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Created On: 10/30/2018
Last Modified: 10/23/2020

Copyright © ABIM Exam World
Created On: 10/30/2018
Last Modified: 10/23/2020

A 19-year-old woman, African American descent, comes to clinic for follow up visit. She has been found to have type 1 diabetes mellitus since the age of 12 years of age. She has been using insulin pump for the last 5 years. She reports no hypoglycemic symptoms and has been monitoring blood sugar using flash glucose monitor. She reports infrequent hypoglycemic episodes all being self-managed. She met with an ophthalmologist for eye screening and has no retinopathy. She exercises regularly for 30 mins. Her vitals recording shows BP of 127/66 mmHg. Her BMI is 22.2.  Systemic  examination is unremarkable. 

Her laboratory investigation is as follows.

What is the MOST LIKELY False statement regarding renal hyper filtration stage of Diabetic Kidney Disease in this patient?

The Correct Answer is Option D : Incretins like GLP-1 and GIP are neutral in terms of altering renal hemodynamics unlike SGLT2 blockers.

Supra-physiologic elevation in GFR is observed early in the natural history of type 1 and type 2 diabetes mellitus which is due to glomerular hyperfiltration. Pathogenesis of hyper filtration in diabetes is complex with a prominent role for hyperglycemia and distorted insulin levels especially in early diabetes and pre-diabetes.Dilatation of the afferent (pre-capillary) glomerular arteriole plays an important role in the hyper-filtration response, by raising both the intra-glomerular pressure and renal blood flow.

The effect of incretins can be demonstrated by experiment using GLP-1 receptor agonists (GLP-1RA) and dipeptidyl peptidase (DPP)–4 inhibitors which are associated with renal hemodynamic effects, potentially beyond glycemic control. These observations have been attributed to a GLP-1–mediated inhibition of NHE3 (which assembles with DPP-4 in the proximal tubular brush border), thereby reducing proximal sodium reabsorption and GFR through activation of TGF (tubuloglomerular feedback).

Option A :  In an 8-week study, empagliflozin in T1DM patients with whole-kidney hyper filtration (mean GFR 172±23 ml/min per 1.73 m2) demonstrated a glucose-independent 19%decrease in GFR, which was associated with a decline in ERPF (estimated renal plasma flow) and estimated glomerular pressure and increase in afferent arteriolar resistance, as assessed by the Gomez equations. SGLT2 inhibition could reduce (single-nephron) hyperfiltration in diabetes by restoring sodium-chloride concentration at the macula densa and subsequent TGF mediated afferent arteriolar vasoconstriction.

Option B : Reported prevalence of hyper filtration at the whole-kidney level vary greatly: between 10% and 67% in type 1 diabetes mellitus (T1DM) (with GFR values up to 162 ml/min per 1.73 m2), and 6%–73% in patients with type 2 diabetes (T2DM) (up to 166 ml/min per 1.73 sq. m. 

Option C: Independent of diabetes and glucose levels, body weight also augments GFR (by about 15% in obese to about 56% in severely obese non-diabetic subjects).

Copyright © ABIM Exam World
Created On: 10/31/2018
Last Modified: 10/23/2020

A 19-year-old woman, African American descent, comes to clinic for follow up visit. She has been found to have type 1 diabetes mellitus since the age of 12 years of age. She has been using insulin pump for the last 5 years. She reports no hypoglycemic symptoms and has been monitoring blood sugar using flash glucose monitor. She reports infrequent hypoglycemic episodes all being self-managed. She met with an ophthalmologist for eye screening and has no retinopathy. She exercises regularly for 30 mins. Her vitals recording shows BP of 127/66 mmHg. Her BMI is 22.2.  Systemic  examination is unremarkable. 

Her laboratory investigation is as follows.

What is the MOST LIKELY False statement regarding renal hyper filtration stage of Diabetic Kidney Disease in this patient?

The Correct Answer is Option D : Incretins like GLP-1 and GIP are neutral in terms of altering renal hemodynamics unlike SGLT2 blockers.

Supra-physiologic elevation in GFR is observed early in the natural history of type 1 and type 2 diabetes mellitus which is due to glomerular hyperfiltration. Pathogenesis of hyper filtration in diabetes is complex with a prominent role for hyperglycemia and distorted insulin levels especially in early diabetes and pre-diabetes.Dilatation of the afferent (pre-capillary) glomerular arteriole plays an important role in the hyper-filtration response, by raising both the intra-glomerular pressure and renal blood flow.

The effect of incretins can be demonstrated by experiment using GLP-1 receptor agonists (GLP-1RA) and dipeptidyl peptidase (DPP)–4 inhibitors which are associated with renal hemodynamic effects, potentially beyond glycemic control. These observations have been attributed to a GLP-1–mediated inhibition of NHE3 (which assembles with DPP-4 in the proximal tubular brush border), thereby reducing proximal sodium reabsorption and GFR through activation of TGF (tubuloglomerular feedback).

Option A :  In an 8-week study, empagliflozin in T1DM patients with whole-kidney hyper filtration (mean GFR 172±23 ml/min per 1.73 m2) demonstrated a glucose-independent 19%decrease in GFR, which was associated with a decline in ERPF (estimated renal plasma flow) and estimated glomerular pressure and increase in afferent arteriolar resistance, as assessed by the Gomez equations. SGLT2 inhibition could reduce (single-nephron) hyperfiltration in diabetes by restoring sodium-chloride concentration at the macula densa and subsequent TGF mediated afferent arteriolar vasoconstriction.

Option B : Reported prevalence of hyper filtration at the whole-kidney level vary greatly: between 10% and 67% in type 1 diabetes mellitus (T1DM) (with GFR values up to 162 ml/min per 1.73 m2), and 6%–73% in patients with type 2 diabetes (T2DM) (up to 166 ml/min per 1.73 sq. m. 

Option C: Independent of diabetes and glucose levels, body weight also augments GFR (by about 15% in obese to about 56% in severely obese non-diabetic subjects).

Copyright © ABIM Exam World
Created On: 10/31/2018
Last Modified: 10/23/2020

A 68-year-old gentleman, Caucasian descent, comes to clinic for follow up visit. He is known to have type 2 diabetes mellitus for the past 18 years. His father had diabetes from 40 years of age and developed kidney disease requiring dialysis after 15 years of diabetes. He reports no symptoms. He has been having hypertension and coronary artery disease with history of  PCI 2 years ago. He has non-proliferative diabetic retinopathy. His medications are sitagliptin, gliclazide and metformin in addition to losartan and hydrochlorothiazide. He has been monitoring blood sugar at home and reports no hypoglycemia. He exercises at least at least 30 minutes per day. His vitals recording shows BP of 168/66 mm Hg. His BMI is 29.2.  Systemic  examination is unremarkable.

His laboratory investigation is reported as follows.

What is the MOST LIKELY correct statement regarding clinical diagnosis of Diabetic Kidney Disease in this patient ?

The Correct Answer is Option D: Family history of Diabetic Kidney Disease is associated with renal involvement in Diabetes.

 Explanation:

Familial studies have demonstrated clustering of diabetic nephropathy. Patients with DM with a first-degree relative with T1/T2DM and diabetic nephropathy have more risk for developing diabetic nephropathy than those without an affected relative. This familial clustering has also been well documented in the Pima Indian population. The candidate genes identified are glucose transporter 2(GLUT2), transforming growth factor beta (TGF- ?), and endothelial nitric oxide synthase (eNOS). 

Option A:  Diabetic nephropathy is a clinical syndrome characterized by the following:

·         Persistent albuminuria (>300 mg/d) that is confirmed on at least 2 occasions 3-6 months apart

·         Progressive decline in the glomerular filtration rate (GFR)

·         Elevated arterial blood pressure 

 Hence kidney biopsy is not a mandatory investigation to diagnose diabetic kidney disease.

 Option B:  If the amount of urine albumin exceeds 30 mg/d and is less than 300 mg/d it is called microalbuminuria, and if it is greater than 300 mg/d it is called macro albuminuria or overt albuminuria. Microalbuminuria is present in 5-7% of normal individuals and is associated with cardiovascular mortality and morbidity. It is marker of endothelial dysfunction in type 2 diabetes mellitus. Presence of microalbuminuria alone with diabetes cannot be clinically diagnostic of diabetic kidney disease.

Option C:  Micro hematuria has been demonstrated in biopsy studies with isolated diabetic nephropathy. Red blood cell casts have also been described in patients with diabetic nephropathy. However, it is important to rule out other glomerular and extra-glomerular causes of hematuria.

Copyright © ABIM Exam World
Created On: 10/31/2018

A 68-year-old gentleman, Caucasian descent, comes to clinic for follow up visit. He is known to have type 2 diabetes mellitus for the past 18 years. His father had diabetes from 40 years of age and developed kidney disease requiring dialysis after 15 years of diabetes. He reports no symptoms. He has been having hypertension and coronary artery disease with history of  PCI 2 years ago. He has non-proliferative diabetic retinopathy. His medications are sitagliptin, gliclazide and metformin in addition to losartan and hydrochlorothiazide. He has been monitoring blood sugar at home and reports no hypoglycemia. He exercises at least at least 30 minutes per day. His vitals recording shows BP of 168/66 mm Hg. His BMI is 29.2.  Systemic  examination is unremarkable.

His laboratory investigation is reported as follows.

What is the MOST LIKELY correct statement regarding clinical diagnosis of Diabetic Kidney Disease in this patient ?

The Correct Answer is Option D: Family history of Diabetic Kidney Disease is associated with renal involvement in Diabetes.

 Explanation:

Familial studies have demonstrated clustering of diabetic nephropathy. Patients with DM with a first-degree relative with T1/T2DM and diabetic nephropathy have more risk for developing diabetic nephropathy than those without an affected relative. This familial clustering has also been well documented in the Pima Indian population. The candidate genes identified are glucose transporter 2(GLUT2), transforming growth factor beta (TGF- ?), and endothelial nitric oxide synthase (eNOS). 

Option A:  Diabetic nephropathy is a clinical syndrome characterized by the following:

·         Persistent albuminuria (>300 mg/d) that is confirmed on at least 2 occasions 3-6 months apart

·         Progressive decline in the glomerular filtration rate (GFR)

·         Elevated arterial blood pressure 

 Hence kidney biopsy is not a mandatory investigation to diagnose diabetic kidney disease.

 Option B:  If the amount of urine albumin exceeds 30 mg/d and is less than 300 mg/d it is called microalbuminuria, and if it is greater than 300 mg/d it is called macro albuminuria or overt albuminuria. Microalbuminuria is present in 5-7% of normal individuals and is associated with cardiovascular mortality and morbidity. It is marker of endothelial dysfunction in type 2 diabetes mellitus. Presence of microalbuminuria alone with diabetes cannot be clinically diagnostic of diabetic kidney disease.

Option C:  Micro hematuria has been demonstrated in biopsy studies with isolated diabetic nephropathy. Red blood cell casts have also been described in patients with diabetic nephropathy. However, it is important to rule out other glomerular and extra-glomerular causes of hematuria.

Copyright © ABIM Exam World
Created On: 10/31/2018

A 30-year-old man was on hemodialysis for 6 months. The was an IV drug user and was diagnosed to have HIV. His elder sister comes forward as protentional kidney donor for him. He underwent a successful kidney transplant. Which of the following statements is true regarding kidney transplantation in HIV positive individuals and acute rejection episodes? 

Correct Answer. Option A. The episodes of acute rejection are more in HIV positive individuals compared to non-HIV positive patients. 

Explanation. 

Kidney transplant recipients with HIV have a high frequency of rejection. In a large, multicenter trial, one- and three-year rejection rates were 31 and 41 %, respectively, compared with an expected one-year rejection rate of 12 percent, as reported by SRTR for all kidney transplant recipients. At European transplant centers, where most patients are induced with interleukin (IL)-2 receptor antibodies, one-year, acute rejection rates among recipients with HIV have ranged from 15 to 44 %.

The higher rate of rejection in recipients with HIV is likely multifactorial. Drug-drug interactions between calcineurin inhibitors (CNIs) and protease inhibitors (PIs) can lead to subtherapeutic exposure to immunosuppressive agents. Patients on a CNI and PI require nonstandard dosing schedules (i.e. every other or every third day), which can make patient adherence difficult. Furthermore, concomitant administration of a PI and CNI results in a 40 % lower area under the curve (AUC) for CNI exposure at the same CNI target level, leading clinicians to systematically underdose patients taking both medications. Many transplant physicians seek to transition patients off PI-based regimens whenever possible in favor of integrase inhibitor-based regimens, which avoid these drug-drug interactions and permit standard immunosuppression dosing.

HIV-infected transplant recipients, compared with HIV-negative recipients, have a higher risk of acute rejection and, therefore, would theoretically benefit from antibody induction therapy. However, given the underlying immunosuppressed state of HIV-infected patients, prolonged lymphocyte depletion with antibody induction therapy could potentially increase their risk of developing opportunistic infections. Some centers avoid the use of antibody induction therapy among HIV-infected transplant recipients. In centers that use antibody induction therapy, some use basiliximab (an IL-2 receptor antibody) based upon data from two studies of HIV-infected kidney transplant recipients that demonstrated an increased risk of infection among those treated with rATG-Thymoglobulin. Other centers prefer to use rATG-Thymoglobulin given its superior efficacy in preventing acute rejection in HIV-negative recipients.

Copyright © ABIM Exam World
Created On: 05/12/2020
Last Modified: 01/28/2021

A 30-year-old man was on hemodialysis for 6 months. The was an IV drug user and was diagnosed to have HIV. His elder sister comes forward as protentional kidney donor for him. He underwent a successful kidney transplant. Which of the following statements is true regarding kidney transplantation in HIV positive individuals and acute rejection episodes? 

Correct Answer. Option A. The episodes of acute rejection are more in HIV positive individuals compared to non-HIV positive patients. 

Explanation. 

Kidney transplant recipients with HIV have a high frequency of rejection. In a large, multicenter trial, one- and three-year rejection rates were 31 and 41 %, respectively, compared with an expected one-year rejection rate of 12 percent, as reported by SRTR for all kidney transplant recipients. At European transplant centers, where most patients are induced with interleukin (IL)-2 receptor antibodies, one-year, acute rejection rates among recipients with HIV have ranged from 15 to 44 %.

The higher rate of rejection in recipients with HIV is likely multifactorial. Drug-drug interactions between calcineurin inhibitors (CNIs) and protease inhibitors (PIs) can lead to subtherapeutic exposure to immunosuppressive agents. Patients on a CNI and PI require nonstandard dosing schedules (i.e. every other or every third day), which can make patient adherence difficult. Furthermore, concomitant administration of a PI and CNI results in a 40 % lower area under the curve (AUC) for CNI exposure at the same CNI target level, leading clinicians to systematically underdose patients taking both medications. Many transplant physicians seek to transition patients off PI-based regimens whenever possible in favor of integrase inhibitor-based regimens, which avoid these drug-drug interactions and permit standard immunosuppression dosing.

HIV-infected transplant recipients, compared with HIV-negative recipients, have a higher risk of acute rejection and, therefore, would theoretically benefit from antibody induction therapy. However, given the underlying immunosuppressed state of HIV-infected patients, prolonged lymphocyte depletion with antibody induction therapy could potentially increase their risk of developing opportunistic infections. Some centers avoid the use of antibody induction therapy among HIV-infected transplant recipients. In centers that use antibody induction therapy, some use basiliximab (an IL-2 receptor antibody) based upon data from two studies of HIV-infected kidney transplant recipients that demonstrated an increased risk of infection among those treated with rATG-Thymoglobulin. Other centers prefer to use rATG-Thymoglobulin given its superior efficacy in preventing acute rejection in HIV-negative recipients.

Copyright © ABIM Exam World
Created On: 05/12/2020
Last Modified: 01/28/2021

A 50-year-old male is referred to for evaluation of high-grade proteinuria. He is not a diabetic but is known to have hypertension. He takes hydrochlorothiazide 12.5 mg once daily for that. The blood and urine tests are shown below. You perform a kidney biopsy and it shows focal segmental glomerulosclerosis (FSGS). The concern is whether this is primary vs. secondary FSGS. Which of the following options would be supportive of secondary FSGS as opposed to primary FSGS? 

Correct Answer. Option C. Serum albumin and width of foot processes (effacement of foot processes).

Explanation. 

The causes of FSGS may be primary (idiopathic) or secondary. The secondary forms are generally characterized by glomerular hyperfiltration and glomerular hypertrophy. It was suggested that serum albumin and the degree of foot processes effacement can distinguish primary from secondary forms of FSGS. Praga et al. reported that serum albumin levels are <3 g/dL in those with biopsy proven primary FSGS, compared to

>3.5 g/dL in those patients with secondary FSGS. A histopathologic study by Deegens et al. showed that the width of foot processes is significantly higher (3200 nm) in primary FSGS, as compared with 1098 nm in secondary FSGS (normal 562 nm). Overall, foot process width over 1500 nm differentiated idiopathic from secondary FSGS with high sensitivity and specificity. This signifies that patients with primary FSGS have complete effacement of foot processes compared to patchy effacement in secondary FSGS. 

In a study of 46 patients with an FSGS lesion, patients were divided by the degree of foot process effacement observed on kidney biopsy. Patients were categorized as having diffuse (?80 %) or limited (<80 %) foot process effacement. Compared with patients with limited foot process effacement, those with diffuse foot process effacement without an identifiable cause had lower serum albumin levels and higher proteinuria and were more likely to have nephrotic syndrome on presentation (100 vs 4 %). Based upon these results, patients who presented with diffuse foot process effacement without an identifiable cause and nephrotic syndrome were classified as primary FSGS. Patients with segmental foot process effacement, with or without an identifiable cause, or diffuse foot process effacement due to an identifiable cause were classified as secondary FSGS.

Copyright © ABIM Exam World
Created On: 05/19/2020
Last Modified: 01/28/2021

A 50-year-old male is referred to for evaluation of high-grade proteinuria. He is not a diabetic but is known to have hypertension. He takes hydrochlorothiazide 12.5 mg once daily for that. The blood and urine tests are shown below. You perform a kidney biopsy and it shows focal segmental glomerulosclerosis (FSGS). The concern is whether this is primary vs. secondary FSGS. Which of the following options would be supportive of secondary FSGS as opposed to primary FSGS? 

Correct Answer. Option C. Serum albumin and width of foot processes (effacement of foot processes).

Explanation. 

The causes of FSGS may be primary (idiopathic) or secondary. The secondary forms are generally characterized by glomerular hyperfiltration and glomerular hypertrophy. It was suggested that serum albumin and the degree of foot processes effacement can distinguish primary from secondary forms of FSGS. Praga et al. reported that serum albumin levels are <3 g/dL in those with biopsy proven primary FSGS, compared to

>3.5 g/dL in those patients with secondary FSGS. A histopathologic study by Deegens et al. showed that the width of foot processes is significantly higher (3200 nm) in primary FSGS, as compared with 1098 nm in secondary FSGS (normal 562 nm). Overall, foot process width over 1500 nm differentiated idiopathic from secondary FSGS with high sensitivity and specificity. This signifies that patients with primary FSGS have complete effacement of foot processes compared to patchy effacement in secondary FSGS. 

In a study of 46 patients with an FSGS lesion, patients were divided by the degree of foot process effacement observed on kidney biopsy. Patients were categorized as having diffuse (?80 %) or limited (<80 %) foot process effacement. Compared with patients with limited foot process effacement, those with diffuse foot process effacement without an identifiable cause had lower serum albumin levels and higher proteinuria and were more likely to have nephrotic syndrome on presentation (100 vs 4 %). Based upon these results, patients who presented with diffuse foot process effacement without an identifiable cause and nephrotic syndrome were classified as primary FSGS. Patients with segmental foot process effacement, with or without an identifiable cause, or diffuse foot process effacement due to an identifiable cause were classified as secondary FSGS.

Copyright © ABIM Exam World
Created On: 05/19/2020
Last Modified: 01/28/2021

A 35 year-old Caucasian male presents with persistent swelling of both legs associated with dark colored urine for two months. He went to an emergency room 2 months ago for these complaints and was told that he has some protein and blood in the urine. He was treated with 3 days of levofloxacin. There is no other past medical history. No history of skin rash or joint swelling. On examination the blood pressure was 130/85 mm Hg and there was bilateral 1+ pedal edema. Rest of the physical examination was normal. Urine analysis showed 3+ proteinuria, 10-15 RBCs per high-power field, and occasional RBC cast. The BUN was 10 mg/dL, serum creatinine was 0.9 mg/dL. Antistreptolysin was negative, C3 level is decreased and C4 level is normal. Antinuclear antibodies, ANCA, hepatitis B and C serology were negative. 24-hour urine collection showed 2 g proteinuria and a kidney biopsy was performed. On light microscopy, kidney biopsy showed increase in the mesangial matrix and cellularity and glomerular basement membrane appeared irregularly thickened. Silver stain revealed duplication of glomerular basement membrane in multiple glomeruli. Immunofluorescence showed positive staining for C3, but negative for IgG, IgM and IgA. Electron microscopy revealed electron-dense deposits in the mesangium and sub-endothelial area. 

What is the most likely diagnosis?

Copyright © ABIM Exam World
Created On: 09/12/2017
Last Modified: 03/07/2021

A 35 year-old Caucasian male presents with persistent swelling of both legs associated with dark colored urine for two months. He went to an emergency room 2 months ago for these complaints and was told that he has some protein and blood in the urine. He was treated with 3 days of levofloxacin. There is no other past medical history. No history of skin rash or joint swelling. On examination the blood pressure was 130/85 mm Hg and there was bilateral 1+ pedal edema. Rest of the physical examination was normal. Urine analysis showed 3+ proteinuria, 10-15 RBCs per high-power field, and occasional RBC cast. The BUN was 10 mg/dL, serum creatinine was 0.9 mg/dL. Antistreptolysin was negative, C3 level is decreased and C4 level is normal. Antinuclear antibodies, ANCA, hepatitis B and C serology were negative. 24-hour urine collection showed 2 g proteinuria and a kidney biopsy was performed. On light microscopy, kidney biopsy showed increase in the mesangial matrix and cellularity and glomerular basement membrane appeared irregularly thickened. Silver stain revealed duplication of glomerular basement membrane in multiple glomeruli. Immunofluorescence showed positive staining for C3, but negative for IgG, IgM and IgA. Electron microscopy revealed electron-dense deposits in the mesangium and sub-endothelial area. 

What is the most likely diagnosis?

Copyright © ABIM Exam World
Created On: 09/12/2017
Last Modified: 03/07/2021

A 25 year-old male comes to the physician complaining of flank pain and hematuria.  He says the pain is constant and dull. There is no frequency, urgency or dysuria.  He has a history of mental retardation and seizures. On physical exam his blood pressure is 140/90 mm Hg, and his pulse is 80 bpm. He has multiple yellow papules across his nose and cheeks and numerous areas of blanched skin spots on his face. A 2-3 cm hypopigmented macule is noted on the right arm. CT scan of the head was done as patient presented with seizures. CT head was reported normal. CT scan of the abdomen shows bilateral hypodense fat containing renal masses and cysts. 

What is the MOST likely diagnosis associated with these findings?

Copyright © ABIM Exam World
Created On: 09/13/2017
Last Modified: 12/30/2017

A 25 year-old male comes to the physician complaining of flank pain and hematuria.  He says the pain is constant and dull. There is no frequency, urgency or dysuria.  He has a history of mental retardation and seizures. On physical exam his blood pressure is 140/90 mm Hg, and his pulse is 80 bpm. He has multiple yellow papules across his nose and cheeks and numerous areas of blanched skin spots on his face. A 2-3 cm hypopigmented macule is noted on the right arm. CT scan of the head was done as patient presented with seizures. CT head was reported normal. CT scan of the abdomen shows bilateral hypodense fat containing renal masses and cysts. 

What is the MOST likely diagnosis associated with these findings?

Copyright © ABIM Exam World
Created On: 09/13/2017
Last Modified: 12/30/2017

A 68 year-old African American male with known history of diabetes mellitus,  hyperlipidemia, CVD, and GERD presents to the ER with chest pain and shortness of breath. Patient says the pain is a crushing pain and radiating to his left arm. It woke him from sleep 30 minutes ago. He took his antacids and 4 tablets of nitroglycerin, and the pain got better. His current medications include low dose aspirin, metoprolol, glyburide, pioglitazone, lisinopril, simvastatin, and omeprazole. He recently suffered an upper respiratory infection for which he was given Levofloxacin. Vitals show: BP 160/95 mm Hg, T 98.1, and HR 110. He has no edema legs and no jugular venous distention. EKG shows LVH by voltage criteria with isoelectric ST segment. Serial troponin levels are normal. A stress test showed evidence of stress inducible ischemia in the anterior leads. He is scheduled for cardiac catheterization the next day. Laboratory results are as follows:

Serum Chemistry:

Na   143 mEq/L

K   3.5 mEq/L

Cl   101 mEq/L

HCO3  22 mEq/L

BUN   35 mg/dL

Cr   3.0 mg/dL

Glucose  110 mg/dL 

What would you do to PROTECT the kidneys before doing the cardiac catheterization?

• Low fractional excretion of sodium (FeNa) below 1%.
• Iodinated contrast agents test false positive for protein and hence proteinuria gets overestimated
• It is reversible most of the time
• UA may show muddy brown granular casts, tubular epithelial cell casts and numerous tubular epithelial casts.

• Chronic kidney disease
• Diabetes mellitus
• Congestive heart failure
• Myeloma kidney
• Hypotension

Copyright © ABIM Exam World
Created On: 09/14/2017
Last Modified: 08/06/2018

A 68 year-old African American male with known history of diabetes mellitus,  hyperlipidemia, CVD, and GERD presents to the ER with chest pain and shortness of breath. Patient says the pain is a crushing pain and radiating to his left arm. It woke him from sleep 30 minutes ago. He took his antacids and 4 tablets of nitroglycerin, and the pain got better. His current medications include low dose aspirin, metoprolol, glyburide, pioglitazone, lisinopril, simvastatin, and omeprazole. He recently suffered an upper respiratory infection for which he was given Levofloxacin. Vitals show: BP 160/95 mm Hg, T 98.1, and HR 110. He has no edema legs and no jugular venous distention. EKG shows LVH by voltage criteria with isoelectric ST segment. Serial troponin levels are normal. A stress test showed evidence of stress inducible ischemia in the anterior leads. He is scheduled for cardiac catheterization the next day. Laboratory results are as follows:

Serum Chemistry:

Na   143 mEq/L

K   3.5 mEq/L

Cl   101 mEq/L

HCO3  22 mEq/L

BUN   35 mg/dL

Cr   3.0 mg/dL

Glucose  110 mg/dL 

What would you do to PROTECT the kidneys before doing the cardiac catheterization?

• Low fractional excretion of sodium (FeNa) below 1%.
• Iodinated contrast agents test false positive for protein and hence proteinuria gets overestimated
• It is reversible most of the time
• UA may show muddy brown granular casts, tubular epithelial cell casts and numerous tubular epithelial casts.

• Chronic kidney disease
• Diabetes mellitus
• Congestive heart failure
• Myeloma kidney
• Hypotension

Copyright © ABIM Exam World
Created On: 09/14/2017
Last Modified: 08/06/2018

A 56 year-old male was brought to the emergency room with drowsiness and lethargy. He has been experiencing these for the last 2 days. He complains of a recent history of anorexia, nausea, and vomiting, He has diabetes mellitus and is on glimepiride 1 mg daily for the last 4 years. One week ago he had decreased vision with redness in his right eye. He was treated by his ophthalmologist with drops which seem to have resolved the problem. He currently takes cholecalciferol weekly for osteoporosis. On physical examination his pulse is 80/min, blood pressure is 140/90 mm Hg, respiratory rate is 20/min, and temperature is 97.7 F. The patient appears drowsy but shows no focal neurological deficits. Review of systems is otherwise unremarkable. Urinalysis is positive for glucose and negative for proteinuria, WBCs and RBC casts. A 24 hour urinary protein collection is significant for proteinuria of 3.5 g/day. Further labs reveal:

Hemoglobin  8 gm%

Hct    24%

MCV   85

WBC   7800/ml

PMN   80%

Lymphocytes  20%

ESR   80 mm/hr

Na    145 mEq/L

BUN   80 mg/dL

Cr    1.8 mg/dL

CL    115 mEq/L

HCO3   25 mEq/L

Uric acid   5.8 mg/dL

Ca    14 mg/dl

PO4    2.8 mg/dL

Total Protein  7.8 gm/dL

Albumin   3.5 mg/dL.

Vitamin D  40 ng/ml

PTH   10 pg/ml

Which of the following is most likely the cause of his hypercalcemia?

• Advanced Age

• Backache and Bone pain

• Anemia

• High ESR

• Urine protein negative by dipstick and positive by other tests is characteristic of light chain proteinuria.

• High Total protein

• Low anion gap

• Hypercalcemia and hyperuricemia favors the diagnosis of multiple myeloma.

Copyright © ABIM Exam World
Created On: 09/20/2017
Last Modified: 08/06/2018

A 56 year-old male was brought to the emergency room with drowsiness and lethargy. He has been experiencing these for the last 2 days. He complains of a recent history of anorexia, nausea, and vomiting, He has diabetes mellitus and is on glimepiride 1 mg daily for the last 4 years. One week ago he had decreased vision with redness in his right eye. He was treated by his ophthalmologist with drops which seem to have resolved the problem. He currently takes cholecalciferol weekly for osteoporosis. On physical examination his pulse is 80/min, blood pressure is 140/90 mm Hg, respiratory rate is 20/min, and temperature is 97.7 F. The patient appears drowsy but shows no focal neurological deficits. Review of systems is otherwise unremarkable. Urinalysis is positive for glucose and negative for proteinuria, WBCs and RBC casts. A 24 hour urinary protein collection is significant for proteinuria of 3.5 g/day. Further labs reveal:

Hemoglobin  8 gm%

Hct    24%

MCV   85

WBC   7800/ml

PMN   80%

Lymphocytes  20%

ESR   80 mm/hr

Na    145 mEq/L

BUN   80 mg/dL

Cr    1.8 mg/dL

CL    115 mEq/L

HCO3   25 mEq/L

Uric acid   5.8 mg/dL

Ca    14 mg/dl

PO4    2.8 mg/dL

Total Protein  7.8 gm/dL

Albumin   3.5 mg/dL.

Vitamin D  40 ng/ml

PTH   10 pg/ml

Which of the following is most likely the cause of his hypercalcemia?

• Advanced Age

• Backache and Bone pain

• Anemia

• High ESR

• Urine protein negative by dipstick and positive by other tests is characteristic of light chain proteinuria.

• High Total protein

• Low anion gap

• Hypercalcemia and hyperuricemia favors the diagnosis of multiple myeloma.

Copyright © ABIM Exam World
Created On: 09/20/2017
Last Modified: 08/06/2018

A 25 year-old female is referred by her primary care provider for evaluation of hypertension and hypokalemia. The primary care provider has already started her on oral potassium, despite therapy her Potassium being 2.8 meq/L. Her blood pressure despite treatment with amlodipine and Lisinopril 154/96 mm of Hg. There is no renal bruit. Systemic and fundus examinations are normal. Her mother was also diagnosed with hypertension at an early age. Her brother died of a cerebrovascular accident 2 years ago. Laboratory findings are as follows:

Na   140 

Potassium 2.8 

Chloride   100 

HCO3    26

BUN   15 

Creatinine  0.8 

Glucose    110

TSH and Cortisol are normal

ACTH    elevated

Renin   0.7 (Low)

Aldosterone  48 (elevated)

Urinalysis:

Sodium   240 mEq/D

Potassium  98 mEq/D

Urinary 18-OH Cortisol and 18-oxocortisol are elevated.

The most appropriate treatment for this patient is:

Copyright © ABIM Exam World
Created On: 09/20/2017
Last Modified: 08/06/2018

A 25 year-old female is referred by her primary care provider for evaluation of hypertension and hypokalemia. The primary care provider has already started her on oral potassium, despite therapy her Potassium being 2.8 meq/L. Her blood pressure despite treatment with amlodipine and Lisinopril 154/96 mm of Hg. There is no renal bruit. Systemic and fundus examinations are normal. Her mother was also diagnosed with hypertension at an early age. Her brother died of a cerebrovascular accident 2 years ago. Laboratory findings are as follows:

Na   140 

Potassium 2.8 

Chloride   100 

HCO3    26

BUN   15 

Creatinine  0.8 

Glucose    110

TSH and Cortisol are normal

ACTH    elevated

Renin   0.7 (Low)

Aldosterone  48 (elevated)

Urinalysis:

Sodium   240 mEq/D

Potassium  98 mEq/D

Urinary 18-OH Cortisol and 18-oxocortisol are elevated.

The most appropriate treatment for this patient is:

Copyright © ABIM Exam World
Created On: 09/20/2017
Last Modified: 08/06/2018

A 60 year-old with recently diagnosed colon cancer and diabetes presents with bilateral pedal edema, BP is 120/80 mm Hg, Urinalysis showed  4+ protein, no RBCs or WBCs, and 8-10 Hyaline casts. His BUN is 20, Creatinine is 1 mg/dL, and albumin is 2 grams/dL. 24 hour urine collection showed 10 grams protein. The patient undergoes kidney biopsy. The EM is shown below :

What is the most likely diagnosis?

The correct answer is E

Membranous Nephropathy.

The Electron microscopy shows subepithelial electron dense deposit as classically seen in membranous nephropathy. If in the question there is a suggestion of colon, breast, or lung cancer, then the glomerulopathy is usually membranous. After that look for other findings on histopathology which will confirm the diagnosis. Subepithelial electron dense deposits.

Explanation:

BOARD POINT - FAMILIARIZE YOURSELF WITH THESE ASSOCIATIONS :

1. Solid cancers (colon, breast, lung, renal) plus proteinuria = Membranous nephropathy

2. Hodgkins lymphoma plus proteinuria = Minimal change disease

3. HIV plus proteinuria = Focal segment glomerulosclerosis FSGS

4. Pamidronate plus protenuria = FSGS (rare)

5. Myeloma, no albuminuria on dipstix, but proteinuria on protein/creatinine ratio or 24 hrs urine: Light chain nephropathy

6. Myeloma with non specific proteinuria (on dipstix, urine protein/creatinine ratio and 24 hrs urine): Light chain nephropathy or amyloidosis.

BOARD POINT - FAMILIARIZE YOURSELF WITH THESE HISTOPATHOLOGY ASSOCIATIONS FOR VARIOUS GLOMERULAR DISEASES

Copyright © ABIM Exam World
Created On: 09/20/2017
Last Modified: 08/29/2018

A 60 year-old with recently diagnosed colon cancer and diabetes presents with bilateral pedal edema, BP is 120/80 mm Hg, Urinalysis showed  4+ protein, no RBCs or WBCs, and 8-10 Hyaline casts. His BUN is 20, Creatinine is 1 mg/dL, and albumin is 2 grams/dL. 24 hour urine collection showed 10 grams protein. The patient undergoes kidney biopsy. The EM is shown below :

What is the most likely diagnosis?

The correct answer is E

Membranous Nephropathy.

The Electron microscopy shows subepithelial electron dense deposit as classically seen in membranous nephropathy. If in the question there is a suggestion of colon, breast, or lung cancer, then the glomerulopathy is usually membranous. After that look for other findings on histopathology which will confirm the diagnosis. Subepithelial electron dense deposits.

Explanation:

BOARD POINT - FAMILIARIZE YOURSELF WITH THESE ASSOCIATIONS :

1. Solid cancers (colon, breast, lung, renal) plus proteinuria = Membranous nephropathy

2. Hodgkins lymphoma plus proteinuria = Minimal change disease

3. HIV plus proteinuria = Focal segment glomerulosclerosis FSGS

4. Pamidronate plus protenuria = FSGS (rare)

5. Myeloma, no albuminuria on dipstix, but proteinuria on protein/creatinine ratio or 24 hrs urine: Light chain nephropathy

6. Myeloma with non specific proteinuria (on dipstix, urine protein/creatinine ratio and 24 hrs urine): Light chain nephropathy or amyloidosis.

BOARD POINT - FAMILIARIZE YOURSELF WITH THESE HISTOPATHOLOGY ASSOCIATIONS FOR VARIOUS GLOMERULAR DISEASES

Copyright © ABIM Exam World
Created On: 09/20/2017
Last Modified: 08/29/2018

A 36 year-old female was diagnosed as having membranous nephropathy secondary to SLE. Her 24 hour protein excretion was 7.5 gms/day. Her serum creatinine was 0.9mg/dl. She was started on 500 mg of cyclophosphamide IV every 15 days (Euro-Lupus) and prednisolone 1 mg/kg orally per day. After 3 months of therapy, she presented with decreased urine output, puffiness of face, and oedema feet. On physical examination, her temperature is 37 C, blood pressure is 160/100 mm Hg, pulse is 90/min, and respiration rate is 20/min. She is anemic and there is puffiness of the face and oedema of the feet. On systemic examination air entry was decreased in the bases of both the lung fields and heart sounds are distant and feeble. Chest X-Ray reveals bilateral pleural effusions. Echocardiogram reveals mild to moderate pericardial effusion. Laboratory examination is as follows: 

Hemoglobin   10.0 g/dL

Hematocrit   34%

Platelet Count   150,000 mm3

WBC    8,000 mm3

Differential count P  80% L 12% E 6% M 2%

ESR    50.8 mm/h

Urinalysis: 

Protein  1450 mg/24 h

Glucose  None

RBCs  70-80/HPF dysmorphic

WBCs  5-8/HPF

Leukocyte Esterase Negative

Nitrites  Negative

 BUN   35 mg/dL

Creatinine  3.9 mg/dL

Sodium   140 mEq/L

Potassium  5.2 mEq/L

Bicarbonate  15.5 mEq/L

Calcium   9.2 mEq/L

Phosphorus  5.6 mg/dL

Glucose   100 mg/dL

Uric Acid   5.3 mg/dL

C3 & C4 decreased 

ANA   positive

dsDNA   positive

Repeat biopsy shows:

Which of the following is the most appropriate therapy for her current condition?

Copyright © ABIM Exam World
Created On: 09/20/2017
Last Modified: 08/06/2018

A 36 year-old female was diagnosed as having membranous nephropathy secondary to SLE. Her 24 hour protein excretion was 7.5 gms/day. Her serum creatinine was 0.9mg/dl. She was started on 500 mg of cyclophosphamide IV every 15 days (Euro-Lupus) and prednisolone 1 mg/kg orally per day. After 3 months of therapy, she presented with decreased urine output, puffiness of face, and oedema feet. On physical examination, her temperature is 37 C, blood pressure is 160/100 mm Hg, pulse is 90/min, and respiration rate is 20/min. She is anemic and there is puffiness of the face and oedema of the feet. On systemic examination air entry was decreased in the bases of both the lung fields and heart sounds are distant and feeble. Chest X-Ray reveals bilateral pleural effusions. Echocardiogram reveals mild to moderate pericardial effusion. Laboratory examination is as follows: 

Hemoglobin   10.0 g/dL

Hematocrit   34%

Platelet Count   150,000 mm3

WBC    8,000 mm3

Differential count P  80% L 12% E 6% M 2%

ESR    50.8 mm/h

Urinalysis: 

Protein  1450 mg/24 h

Glucose  None

RBCs  70-80/HPF dysmorphic

WBCs  5-8/HPF

Leukocyte Esterase Negative

Nitrites  Negative

 BUN   35 mg/dL

Creatinine  3.9 mg/dL

Sodium   140 mEq/L

Potassium  5.2 mEq/L

Bicarbonate  15.5 mEq/L

Calcium   9.2 mEq/L

Phosphorus  5.6 mg/dL

Glucose   100 mg/dL

Uric Acid   5.3 mg/dL

C3 & C4 decreased 

ANA   positive

dsDNA   positive

Repeat biopsy shows:

Which of the following is the most appropriate therapy for her current condition?

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Created On: 09/20/2017
Last Modified: 08/06/2018

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Created On: 10/30/2018
Last Modified: 10/23/2020

Copyright © ABIM Exam World
Created On: 10/30/2018
Last Modified: 10/23/2020

A 19-year-old woman, African American descent, comes to clinic for follow up visit. She has been found to have type 1 diabetes mellitus since the age of 12 years of age. She has been using insulin pump for the last 5 years. She reports no hypoglycemic symptoms and has been monitoring blood sugar using flash glucose monitor. She reports infrequent hypoglycemic episodes all being self-managed. She met with an ophthalmologist for eye screening and has no retinopathy. She exercises regularly for 30 mins. Her vitals recording shows BP of 127/66 mmHg. Her BMI is 22.2.  Systemic  examination is unremarkable. 

Her laboratory investigation is as follows.

What is the MOST LIKELY False statement regarding renal hyper filtration stage of Diabetic Kidney Disease in this patient?

The Correct Answer is Option D : Incretins like GLP-1 and GIP are neutral in terms of altering renal hemodynamics unlike SGLT2 blockers.

Supra-physiologic elevation in GFR is observed early in the natural history of type 1 and type 2 diabetes mellitus which is due to glomerular hyperfiltration. Pathogenesis of hyper filtration in diabetes is complex with a prominent role for hyperglycemia and distorted insulin levels especially in early diabetes and pre-diabetes.Dilatation of the afferent (pre-capillary) glomerular arteriole plays an important role in the hyper-filtration response, by raising both the intra-glomerular pressure and renal blood flow.

The effect of incretins can be demonstrated by experiment using GLP-1 receptor agonists (GLP-1RA) and dipeptidyl peptidase (DPP)–4 inhibitors which are associated with renal hemodynamic effects, potentially beyond glycemic control. These observations have been attributed to a GLP-1–mediated inhibition of NHE3 (which assembles with DPP-4 in the proximal tubular brush border), thereby reducing proximal sodium reabsorption and GFR through activation of TGF (tubuloglomerular feedback).

Option A :  In an 8-week study, empagliflozin in T1DM patients with whole-kidney hyper filtration (mean GFR 172±23 ml/min per 1.73 m2) demonstrated a glucose-independent 19%decrease in GFR, which was associated with a decline in ERPF (estimated renal plasma flow) and estimated glomerular pressure and increase in afferent arteriolar resistance, as assessed by the Gomez equations. SGLT2 inhibition could reduce (single-nephron) hyperfiltration in diabetes by restoring sodium-chloride concentration at the macula densa and subsequent TGF mediated afferent arteriolar vasoconstriction.

Option B : Reported prevalence of hyper filtration at the whole-kidney level vary greatly: between 10% and 67% in type 1 diabetes mellitus (T1DM) (with GFR values up to 162 ml/min per 1.73 m2), and 6%–73% in patients with type 2 diabetes (T2DM) (up to 166 ml/min per 1.73 sq. m. 

Option C: Independent of diabetes and glucose levels, body weight also augments GFR (by about 15% in obese to about 56% in severely obese non-diabetic subjects).

Copyright © ABIM Exam World
Created On: 10/31/2018
Last Modified: 10/23/2020

A 19-year-old woman, African American descent, comes to clinic for follow up visit. She has been found to have type 1 diabetes mellitus since the age of 12 years of age. She has been using insulin pump for the last 5 years. She reports no hypoglycemic symptoms and has been monitoring blood sugar using flash glucose monitor. She reports infrequent hypoglycemic episodes all being self-managed. She met with an ophthalmologist for eye screening and has no retinopathy. She exercises regularly for 30 mins. Her vitals recording shows BP of 127/66 mmHg. Her BMI is 22.2.  Systemic  examination is unremarkable. 

Her laboratory investigation is as follows.

What is the MOST LIKELY False statement regarding renal hyper filtration stage of Diabetic Kidney Disease in this patient?

The Correct Answer is Option D : Incretins like GLP-1 and GIP are neutral in terms of altering renal hemodynamics unlike SGLT2 blockers.

Supra-physiologic elevation in GFR is observed early in the natural history of type 1 and type 2 diabetes mellitus which is due to glomerular hyperfiltration. Pathogenesis of hyper filtration in diabetes is complex with a prominent role for hyperglycemia and distorted insulin levels especially in early diabetes and pre-diabetes.Dilatation of the afferent (pre-capillary) glomerular arteriole plays an important role in the hyper-filtration response, by raising both the intra-glomerular pressure and renal blood flow.

The effect of incretins can be demonstrated by experiment using GLP-1 receptor agonists (GLP-1RA) and dipeptidyl peptidase (DPP)–4 inhibitors which are associated with renal hemodynamic effects, potentially beyond glycemic control. These observations have been attributed to a GLP-1–mediated inhibition of NHE3 (which assembles with DPP-4 in the proximal tubular brush border), thereby reducing proximal sodium reabsorption and GFR through activation of TGF (tubuloglomerular feedback).

Option A :  In an 8-week study, empagliflozin in T1DM patients with whole-kidney hyper filtration (mean GFR 172±23 ml/min per 1.73 m2) demonstrated a glucose-independent 19%decrease in GFR, which was associated with a decline in ERPF (estimated renal plasma flow) and estimated glomerular pressure and increase in afferent arteriolar resistance, as assessed by the Gomez equations. SGLT2 inhibition could reduce (single-nephron) hyperfiltration in diabetes by restoring sodium-chloride concentration at the macula densa and subsequent TGF mediated afferent arteriolar vasoconstriction.

Option B : Reported prevalence of hyper filtration at the whole-kidney level vary greatly: between 10% and 67% in type 1 diabetes mellitus (T1DM) (with GFR values up to 162 ml/min per 1.73 m2), and 6%–73% in patients with type 2 diabetes (T2DM) (up to 166 ml/min per 1.73 sq. m. 

Option C: Independent of diabetes and glucose levels, body weight also augments GFR (by about 15% in obese to about 56% in severely obese non-diabetic subjects).

Copyright © ABIM Exam World
Created On: 10/31/2018
Last Modified: 10/23/2020

A 68-year-old gentleman, Caucasian descent, comes to clinic for follow up visit. He is known to have type 2 diabetes mellitus for the past 18 years. His father had diabetes from 40 years of age and developed kidney disease requiring dialysis after 15 years of diabetes. He reports no symptoms. He has been having hypertension and coronary artery disease with history of  PCI 2 years ago. He has non-proliferative diabetic retinopathy. His medications are sitagliptin, gliclazide and metformin in addition to losartan and hydrochlorothiazide. He has been monitoring blood sugar at home and reports no hypoglycemia. He exercises at least at least 30 minutes per day. His vitals recording shows BP of 168/66 mm Hg. His BMI is 29.2.  Systemic  examination is unremarkable.

His laboratory investigation is reported as follows.

What is the MOST LIKELY correct statement regarding clinical diagnosis of Diabetic Kidney Disease in this patient ?

The Correct Answer is Option D: Family history of Diabetic Kidney Disease is associated with renal involvement in Diabetes.

 Explanation:

Familial studies have demonstrated clustering of diabetic nephropathy. Patients with DM with a first-degree relative with T1/T2DM and diabetic nephropathy have more risk for developing diabetic nephropathy than those without an affected relative. This familial clustering has also been well documented in the Pima Indian population. The candidate genes identified are glucose transporter 2(GLUT2), transforming growth factor beta (TGF- ?), and endothelial nitric oxide synthase (eNOS). 

Option A:  Diabetic nephropathy is a clinical syndrome characterized by the following:

·         Persistent albuminuria (>300 mg/d) that is confirmed on at least 2 occasions 3-6 months apart

·         Progressive decline in the glomerular filtration rate (GFR)

·         Elevated arterial blood pressure 

 Hence kidney biopsy is not a mandatory investigation to diagnose diabetic kidney disease.

 Option B:  If the amount of urine albumin exceeds 30 mg/d and is less than 300 mg/d it is called microalbuminuria, and if it is greater than 300 mg/d it is called macro albuminuria or overt albuminuria. Microalbuminuria is present in 5-7% of normal individuals and is associated with cardiovascular mortality and morbidity. It is marker of endothelial dysfunction in type 2 diabetes mellitus. Presence of microalbuminuria alone with diabetes cannot be clinically diagnostic of diabetic kidney disease.

Option C:  Micro hematuria has been demonstrated in biopsy studies with isolated diabetic nephropathy. Red blood cell casts have also been described in patients with diabetic nephropathy. However, it is important to rule out other glomerular and extra-glomerular causes of hematuria.

Copyright © ABIM Exam World
Created On: 10/31/2018

A 68-year-old gentleman, Caucasian descent, comes to clinic for follow up visit. He is known to have type 2 diabetes mellitus for the past 18 years. His father had diabetes from 40 years of age and developed kidney disease requiring dialysis after 15 years of diabetes. He reports no symptoms. He has been having hypertension and coronary artery disease with history of  PCI 2 years ago. He has non-proliferative diabetic retinopathy. His medications are sitagliptin, gliclazide and metformin in addition to losartan and hydrochlorothiazide. He has been monitoring blood sugar at home and reports no hypoglycemia. He exercises at least at least 30 minutes per day. His vitals recording shows BP of 168/66 mm Hg. His BMI is 29.2.  Systemic  examination is unremarkable.

His laboratory investigation is reported as follows.