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

All of the following are helpful in predicting AV Graft stenosis EXCEPT:

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Created On: 09/14/2017
Last Modified: 08/06/2018

All of the following are helpful in predicting AV Graft stenosis EXCEPT:

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Created On: 09/14/2017
Last Modified: 08/06/2018

Cyclosporine nephrotoxicity in a renal transplant recipient is associated with all the below renal biopsy findings EXCEPT:

(THIS PICTURE BELOW IN LOW POWER SHOWS ONE OF THE CLASSICAL FINDINGS IN CSA TOXICITY)

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Created On: 09/14/2017
Last Modified: 08/06/2018

Cyclosporine nephrotoxicity in a renal transplant recipient is associated with all the below renal biopsy findings EXCEPT:

(THIS PICTURE BELOW IN LOW POWER SHOWS ONE OF THE CLASSICAL FINDINGS IN CSA TOXICITY)

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Created On: 09/14/2017
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

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Created On: 09/20/2017
Last Modified: 08/29/2018

You are the nephrologist on call. The  ER calls you for an 18 year-old female who complaining of vomiting and diarrhea. Her serum sodium is 116 mEq/L and Serum potassium is 5.9 mEq/L. On physical examination the patient is drowsy, Pulse is 126/min, BP is 90/60 mm of Hg, and RR is  32/min. Her chest is clear. Her heart sounds are normal, and no murmur is visible. The patient is drowsy but arousable and there was no focal neurological deficit. Laboratory findings are as follows:

Hb    16 gm/dl 

WBC   12,800/cmm 

Polymorph  46% 

Lymphocytes  16% 

Eosinophils  4%

Monocytes  4%

Platelets   2,40,000/cmm.

CL    70 mEq/L

BUN  10 mg/dl

Creatinine  0.5 mg/dl

Na    116 mEq/L

K    5.8 mEq/L

Urinalysis:

pH    6.4

Protein  trace

Glucose  absent

microscopic occasional WBCs & RBCs

Urinary Na  90 mEq/L

Urinary K         20 mEq/L

ABG    

PH                   7.32

PCO2   36 

HCO3   20 mEq/L

PaO2   92

O2 saturation  98%

S. Cortisol  6.00 mg/dl

TSH   3.5 IU/m (Normal 0-5 IU/m ).

Both plasma Renin and Aldosterone are high. 

Which of the following conditions is most likely with these findings?

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

You are the nephrologist on call. The  ER calls you for an 18 year-old female who complaining of vomiting and diarrhea. Her serum sodium is 116 mEq/L and Serum potassium is 5.9 mEq/L. On physical examination the patient is drowsy, Pulse is 126/min, BP is 90/60 mm of Hg, and RR is  32/min. Her chest is clear. Her heart sounds are normal, and no murmur is visible. The patient is drowsy but arousable and there was no focal neurological deficit. Laboratory findings are as follows:

Hb    16 gm/dl 

WBC   12,800/cmm 

Polymorph  46% 

Lymphocytes  16% 

Eosinophils  4%

Monocytes  4%

Platelets   2,40,000/cmm.

CL    70 mEq/L

BUN  10 mg/dl

Creatinine  0.5 mg/dl

Na    116 mEq/L

K    5.8 mEq/L

Urinalysis:

pH    6.4

Protein  trace

Glucose  absent

microscopic occasional WBCs & RBCs

Urinary Na  90 mEq/L

Urinary K         20 mEq/L

ABG    

PH                   7.32

PCO2   36 

HCO3   20 mEq/L

PaO2   92

O2 saturation  98%

S. Cortisol  6.00 mg/dl

TSH   3.5 IU/m (Normal 0-5 IU/m ).

Both plasma Renin and Aldosterone are high. 

Which of the following conditions is most likely with these findings?

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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?

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

A 30 year-old man comes to your office for a painful rash on the neck. He has fever and malaise. He has history of HIV. He is currently taking Tenofovir, emtricitabine, and indinavir.  The rash is suggestive of Herpes Zoster rash :

Physical examination does not reveal any oral cavity lesions. His current CD4 count is 250/mm3. His chemistry is normal. He is started on an intravenous medication for his rash. Two days later his chemistry is as follows:

Na    135 mEq/L

K     4.5 mEq/L                  

CL    100 mEq/L

HCO3   24 mEq/L                  

BUN  21 mg/dL                       

Cr   2.0 mEq/L

Glucose  95 mg/dL

Calcium   9.4 mg/dl

Urinalysis shows needle-shaped crystals in the sediment.

Which of the following is most likely the cause of his renal problem?

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Created On: 09/20/2017
Last Modified: 08/29/2018

A 30 year-old man comes to your office for a painful rash on the neck. He has fever and malaise. He has history of HIV. He is currently taking Tenofovir, emtricitabine, and indinavir.  The rash is suggestive of Herpes Zoster rash :

Physical examination does not reveal any oral cavity lesions. His current CD4 count is 250/mm3. His chemistry is normal. He is started on an intravenous medication for his rash. Two days later his chemistry is as follows:

Na    135 mEq/L

K     4.5 mEq/L                  

CL    100 mEq/L

HCO3   24 mEq/L                  

BUN  21 mg/dL                       

Cr   2.0 mEq/L

Glucose  95 mg/dL

Calcium   9.4 mg/dl

Urinalysis shows needle-shaped crystals in the sediment.

Which of the following is most likely the cause of his renal problem?

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Created On: 09/20/2017
Last Modified: 08/29/2018

 In a CKD and ESRD patient, Vitamin D seems to protect against cardiovascular disease events by controlling secondary hyperparathyroidism. The OPERA trial evaluated the effect of paricalcitol Vitamin D analog in CKD stages 3-5 with left ventricular hypertrophy. The study observed the effect on left ventricular mass and function.

Which of the following statements is true about the effect of paricalcitol in CKD and ESRD patients?

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

 In a CKD and ESRD patient, Vitamin D seems to protect against cardiovascular disease events by controlling secondary hyperparathyroidism. The OPERA trial evaluated the effect of paricalcitol Vitamin D analog in CKD stages 3-5 with left ventricular hypertrophy. The study observed the effect on left ventricular mass and function.

Which of the following statements is true about the effect of paricalcitol in CKD and ESRD patients?

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

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).

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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).

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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.

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Created On: 10/31/2018

All the following drugs mentioned below cause hyperkalemia. All the drugs act by a specific mechanism to induce hyperkalemia. Only one drug acts by a different mechanism of action. Which is the drug which induces hyperkalemia via a different mechanism than others?  

Correct Answer. Option D. Calcineurin inhibitors. 

Explanation. 

Heparin, Low molecular weight heparin, Aminoglutethimide and Dabigatran all cause impaired adrenal hormone metabolism. These drugs cause potent inhibition of adrenal hormone synthesis leading to hyperkalemia. 

The hyperkalemia seen with calcineurin inhibition is likely multifactorial and relates to inhibitory effects on Na+-K+-ATPase in collecting ducts and possibly to distal tubular acidosis. In addition, there is evidence that decreased numbers of mineralocorticoid receptors, which are detected in 75% of patients who are treated with cyclosporine, lead to hyperkalemia and metabolic acidosis as a result of aldosterone resistance. Recently, it was demonstrated that cyclosporine reduces paracellin-1 expression in thick ascending limb cells. The resulting decrease in magnesium transport likely contributes to the magnesium wasting and hypomagnesemia induced by cyclosporine, which is associated with chronic interstitial fibrosis, a faster rate of decline of kidney function, and increased rates of graft loss in renal transplant recipients with CNI nephrotoxicity. Finally, it was shown that cyclosporine indirectly opens ATP-sensitive K+ channels by inhibition of calcineurin, which could contribute to the CNI-associated hyperkalemia. 

Copyright © ABIM Exam World
Created On: 05/18/2020
Last Modified: 01/28/2021

All the following drugs mentioned below cause hyperkalemia. All the drugs act by a specific mechanism to induce hyperkalemia. Only one drug acts by a different mechanism of action. Which is the drug which induces hyperkalemia via a different mechanism than others?  

Correct Answer. Option D. Calcineurin inhibitors. 

Explanation. 

Heparin, Low molecular weight heparin, Aminoglutethimide and Dabigatran all cause impaired adrenal hormone metabolism. These drugs cause potent inhibition of adrenal hormone synthesis leading to hyperkalemia. 

The hyperkalemia seen with calcineurin inhibition is likely multifactorial and relates to inhibitory effects on Na+-K+-ATPase in collecting ducts and possibly to distal tubular acidosis. In addition, there is evidence that decreased numbers of mineralocorticoid receptors, which are detected in 75% of patients who are treated with cyclosporine, lead to hyperkalemia and metabolic acidosis as a result of aldosterone resistance. Recently, it was demonstrated that cyclosporine reduces paracellin-1 expression in thick ascending limb cells. The resulting decrease in magnesium transport likely contributes to the magnesium wasting and hypomagnesemia induced by cyclosporine, which is associated with chronic interstitial fibrosis, a faster rate of decline of kidney function, and increased rates of graft loss in renal transplant recipients with CNI nephrotoxicity. Finally, it was shown that cyclosporine indirectly opens ATP-sensitive K+ channels by inhibition of calcineurin, which could contribute to the CNI-associated hyperkalemia. 

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Created On: 05/18/2020
Last Modified: 01/28/2021

A 68-year-old Hispanic woman is referred to you for evaluation of nephrotic syndrome. She has history of type 2 diabetes and hypertension. Both diabetes and hypertension are well controlled. Her serum creatinine is 2.1 mg/dL. Urinalysis shows only proteinuria, and protein to creatinine ratio is 6. A renal biopsy shows amyloidosis and interstitial fibrosis. Based on the above history, biopsy findings, and proteinuria, which one of the following diagnostic tests you order to characterize the type of her amyloidosis?

Correct Answer. Option D. Amyloidosis derived from leukocyte chemotactic factor 2 (ALECT 2).

Explanation. 

ALECT2 amyloidosis is a systemic form of amyloidosis with predominantly renal and liver involvement. Most reported cases in North America (88 to 92 %) occur in older Hispanic adults of Mexican origin, although Punjabis, First Nations people in British Columbia, and Native Americans also have a predisposition for this disorder. In one study of renal amyloidosis among Egyptians, ALECT2 amyloidosis was the second most common form of renal amyloidosis behind AA and ahead of AL amyloidosis. Cases have also been reported in Pakistani, Sudanese, and Chinese patients. The pathogenesis of ALECT2 amyloidosis is not well understood. Patients typically present with chronic kidney disease (CKD) and variable proteinuria; nephrotic syndrome is uncommon. A kidney biopsy, preferably with laser microdissection and mass spectrometry, is required to make the diagnosis. Patients with ALECT2 amyloidosis characteristically have diffuse Congo red-positive amyloid deposition in the cortical interstitium, with variable glomerular and vascular involvement. In general, patients with ALECT2 amyloidosis have better overall survival than those with AL or AA amyloidosis, possibly due to the absence or rare occurrence of cardiac involvement. However, renal survival is relatively poor, with up to 39 percent of patients progressing to end-stage renal disease (ESRD). There are no specific therapies for ALECT2 amyloidosis.

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

A 68-year-old Hispanic woman is referred to you for evaluation of nephrotic syndrome. She has history of type 2 diabetes and hypertension. Both diabetes and hypertension are well controlled. Her serum creatinine is 2.1 mg/dL. Urinalysis shows only proteinuria, and protein to creatinine ratio is 6. A renal biopsy shows amyloidosis and interstitial fibrosis. Based on the above history, biopsy findings, and proteinuria, which one of the following diagnostic tests you order to characterize the type of her amyloidosis?

Correct Answer. Option D. Amyloidosis derived from leukocyte chemotactic factor 2 (ALECT 2).

Explanation. 

ALECT2 amyloidosis is a systemic form of amyloidosis with predominantly renal and liver involvement. Most reported cases in North America (88 to 92 %) occur in older Hispanic adults of Mexican origin, although Punjabis, First Nations people in British Columbia, and Native Americans also have a predisposition for this disorder. In one study of renal amyloidosis among Egyptians, ALECT2 amyloidosis was the second most common form of renal amyloidosis behind AA and ahead of AL amyloidosis. Cases have also been reported in Pakistani, Sudanese, and Chinese patients. The pathogenesis of ALECT2 amyloidosis is not well understood. Patients typically present with chronic kidney disease (CKD) and variable proteinuria; nephrotic syndrome is uncommon. A kidney biopsy, preferably with laser microdissection and mass spectrometry, is required to make the diagnosis. Patients with ALECT2 amyloidosis characteristically have diffuse Congo red-positive amyloid deposition in the cortical interstitium, with variable glomerular and vascular involvement. In general, patients with ALECT2 amyloidosis have better overall survival than those with AL or AA amyloidosis, possibly due to the absence or rare occurrence of cardiac involvement. However, renal survival is relatively poor, with up to 39 percent of patients progressing to end-stage renal disease (ESRD). There are no specific therapies for ALECT2 amyloidosis.

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?

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

All of the following are helpful in predicting AV Graft stenosis EXCEPT:

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Created On: 09/14/2017
Last Modified: 08/06/2018

All of the following are helpful in predicting AV Graft stenosis EXCEPT:

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Created On: 09/14/2017
Last Modified: 08/06/2018

Cyclosporine nephrotoxicity in a renal transplant recipient is associated with all the below renal biopsy findings EXCEPT:

(THIS PICTURE BELOW IN LOW POWER SHOWS ONE OF THE CLASSICAL FINDINGS IN CSA TOXICITY)

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

Cyclosporine nephrotoxicity in a renal transplant recipient is associated with all the below renal biopsy findings EXCEPT:

(THIS PICTURE BELOW IN LOW POWER SHOWS ONE OF THE CLASSICAL FINDINGS IN CSA TOXICITY)

Copyright © ABIM Exam World
Created On: 09/14/2017
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

You are the nephrologist on call. The  ER calls you for an 18 year-old female who complaining of vomiting and diarrhea. Her serum sodium is 116 mEq/L and Serum potassium is 5.9 mEq/L. On physical examination the patient is drowsy, Pulse is 126/min, BP is 90/60 mm of Hg, and RR is  32/min. Her chest is clear. Her heart sounds are normal, and no murmur is visible. The patient is drowsy but arousable and there was no focal neurological deficit. Laboratory findings are as follows:

Hb    16 gm/dl 

WBC   12,800/cmm 

Polymorph  46% 

Lymphocytes  16% 

Eosinophils  4%

Monocytes  4%

Platelets   2,40,000/cmm.

CL    70 mEq/L

BUN  10 mg/dl

Creatinine  0.5 mg/dl

Na    116 mEq/L

K    5.8 mEq/L

Urinalysis:

pH    6.4

Protein  trace

Glucose  absent

microscopic occasional WBCs & RBCs

Urinary Na  90 mEq/L

Urinary K         20 mEq/L

ABG    

PH                   7.32

PCO2   36 

HCO3   20 mEq/L

PaO2   92

O2 saturation  98%

S. Cortisol  6.00 mg/dl

TSH   3.5 IU/m (Normal 0-5 IU/m ).

Both plasma Renin and Aldosterone are high. 

Which of the following conditions is most likely with these findings?

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

You are the nephrologist on call. The  ER calls you for an 18 year-old female who complaining of vomiting and diarrhea. Her serum sodium is 116 mEq/L and Serum potassium is 5.9 mEq/L. On physical examination the patient is drowsy, Pulse is 126/min, BP is 90/60 mm of Hg, and RR is  32/min. Her chest is clear. Her heart sounds are normal, and no murmur is visible. The patient is drowsy but arousable and there was no focal neurological deficit. Laboratory findings are as follows:

Hb    16 gm/dl 

WBC   12,800/cmm 

Polymorph  46% 

Lymphocytes  16% 

Eosinophils  4%

Monocytes  4%

Platelets   2,40,000/cmm.

CL    70 mEq/L

BUN  10 mg/dl

Creatinine  0.5 mg/dl

Na    116 mEq/L

K    5.8 mEq/L

Urinalysis:

pH    6.4

Protein  trace

Glucose  absent

microscopic occasional WBCs & RBCs

Urinary Na  90 mEq/L

Urinary K         20 mEq/L

ABG    

PH                   7.32

PCO2   36 

HCO3   20 mEq/L

PaO2   92

O2 saturation  98%

S. Cortisol  6.00 mg/dl

TSH   3.5 IU/m (Normal 0-5 IU/m ).

Both plasma Renin and Aldosterone are high. 

Which of the following conditions is most likely with these findings?

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?

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?

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

A 30 year-old man comes to your office for a painful rash on the neck. He has fever and malaise. He has history of HIV. He is currently taking Tenofovir, emtricitabine, and indinavir.  The rash is suggestive of Herpes Zoster rash :

Physical examination does not reveal any oral cavity lesions. His current CD4 count is 250/mm3. His chemistry is normal. He is started on an intravenous medication for his rash. Two days later his chemistry is as follows:

Na    135 mEq/L

K     4.5 mEq/L                  

CL    100 mEq/L

HCO3   24 mEq/L                  

BUN  21 mg/dL                       

Cr   2.0 mEq/L

Glucose  95 mg/dL

Calcium   9.4 mg/dl

Urinalysis shows needle-shaped crystals in the sediment.

Which of the following is most likely the cause of his renal problem?

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

A 30 year-old man comes to your office for a painful rash on the neck. He has fever and malaise. He has history of HIV. He is currently taking Tenofovir, emtricitabine, and indinavir.  The rash is suggestive of Herpes Zoster rash :

Physical examination does not reveal any oral cavity lesions. His current CD4 count is 250/mm3. His chemistry is normal. He is started on an intravenous medication for his rash. Two days later his chemistry is as follows:

Na    135 mEq/L

K     4.5 mEq/L                  

CL    100 mEq/L

HCO3   24 mEq/L                  

BUN  21 mg/dL                       

Cr   2.0 mEq/L

Glucose  95 mg/dL

Calcium   9.4 mg/dl

Urinalysis shows needle-shaped crystals in the sediment.

Which of the following is most likely the cause of his renal problem?

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Created On: 09/20/2017
Last Modified: 08/29/2018

 In a CKD and ESRD patient, Vitamin D seems to protect against cardiovascular disease events by controlling secondary hyperparathyroidism. The OPERA trial evaluated the effect of paricalcitol Vitamin D analog in CKD stages 3-5 with left ventricular hypertrophy. The study observed the effect on left ventricular mass and function.

Which of the following statements is true about the effect of paricalcitol in CKD and ESRD patients?

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

 In a CKD and ESRD patient, Vitamin D seems to protect against cardiovascular disease events by controlling secondary hyperparathyroidism. The OPERA trial evaluated the effect of paricalcitol Vitamin D analog in CKD stages 3-5 with left ventricular hypertrophy. The study observed the effect on left ventricular mass and function.

Which of the following statements is true about the effect of paricalcitol in CKD and ESRD patients?

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

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.

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Created On: 10/31/2018

All the following drugs mentioned below cause hyperkalemia. All the drugs act by a specific mechanism to induce hyperkalemia. Only one drug acts by a different mechanism of action. Which is the drug which induces hyperkalemia via a different mechanism than others?  

Correct Answer. Option D. Calcineurin inhibitors. 

Explanation. 

Heparin, Low molecular weight heparin, Aminoglutethimide and Dabigatran all cause impaired adrenal hormone metabolism. These drugs cause potent inhibition of adrenal hormone synthesis leading to hyperkalemia. 

The hyperkalemia seen with calcineurin inhibition is likely multifactorial and relates to inhibitory effects on Na+-K+-ATPase in collecting ducts and possibly to distal tubular acidosis. In addition, there is evidence that decreased numbers of mineralocorticoid receptors, which are detected in 75% of patients who are treated with cyclosporine, lead to hyperkalemia and metabolic acidosis as a result of aldosterone resistance. Recently, it was demonstrated that cyclosporine reduces paracellin-1 expression in thick ascending limb cells. The resulting decrease in magnesium transport likely contributes to the magnesium wasting and hypomagnesemia induced by cyclosporine, which is associated with chronic interstitial fibrosis, a faster rate of decline of kidney function, and increased rates of graft loss in renal transplant recipients with CNI nephrotoxicity. Finally, it was shown that cyclosporine indirectly opens ATP-sensitive K+ channels by inhibition of calcineurin, which could contribute to the CNI-associated hyperkalemia. 

Copyright © ABIM Exam World
Created On: 05/18/2020
Last Modified: 01/28/2021

All the following drugs mentioned below cause hyperkalemia. All the drugs act by a specific mechanism to induce hyperkalemia. Only one drug acts by a different mechanism of action. Which is the drug which induces hyperkalemia via a different mechanism than others?  

Correct Answer. Option D. Calcineurin inhibitors. 

Explanation. 

Heparin, Low molecular weight heparin, Aminoglutethimide and Dabigatran all cause impaired adrenal hormone metabolism. These drugs cause potent inhibition of adrenal hormone synthesis leading to hyperkalemia. 

The hyperkalemia seen with calcineurin inhibition is likely multifactorial and relates to inhibitory effects on Na+-K+-ATPase in collecting ducts and possibly to distal tubular acidosis. In addition, there is evidence that decreased numbers of mineralocorticoid receptors, which are detected in 75% of patients who are treated with cyclosporine, lead to hyperkalemia and metabolic acidosis as a result of aldosterone resistance. Recently, it was demonstrated that cyclosporine reduces paracellin-1 expression in thick ascending limb cells. The resulting decrease in magnesium transport likely contributes to the magnesium wasting and hypomagnesemia induced by cyclosporine, which is associated with chronic interstitial fibrosis, a faster rate of decline of kidney function, and increased rates of graft loss in renal transplant recipients with CNI nephrotoxicity. Finally, it was shown that cyclosporine indirectly opens ATP-sensitive K+ channels by inhibition of calcineurin, which could contribute to the CNI-associated hyperkalemia. 

Copyright © ABIM Exam World
Created On: 05/18/2020
Last Modified: 01/28/2021