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.
Characteristic
value
Hemoglobin
12.2 gm/L
WBC count
6.8 X 103/cubic mm
Platelet count
241 X 103/cubic mm
Segmented Neutrophils
Lymphocytes
Monocytes
Band neutrophils
Eosinophils
Basophils
60%
36%
2%
0%
Sr. Sodium
139 mEq/L
Sr. Potassium
4.9 mEq/L
Sr. Creatinine
1.2 mg/dL
Sr. Bicarbonate
22 mEq/L
Sr. Chloride
101 mEq/L
Total Bilirubin
1.0 mg /dL
AST
16 U/L
ALT
18 U/L
Sr. Albumin
4.0 g/dL
HBA1C
7.8%
Sr. Calcium
10 mg/dL
Urine dipstick
pH- 5.4
Albumin-trace
no blood
no WBCs
24-hour urinary albumin
200 milligrams/day
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
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
All of the following are helpful in predicting AV Graft stenosis EXCEPT:
Copyright © ABIM Exam World Created On: 09/23/2020 Last Modified: 01/28/2021
A 40 year-old pleasant African man with ESRD secondary to FSGS started automated peritoneal dialysis. His prescription includes 2.5 L and 3 exchanges over 8 hours at night with a last fill of 2 L. He has a urine output of 1000 mL/day. A typical ultrafiltration on cycler is used at 1000 mL. Average drain volume of the day dwell was 1500 mL prior to going on the cycler at night.
He came with complains of lower abdominal wall edema extending to the scrotum over the past 5 days. Without any change in the dialysis prescription, his drain volume before going on the cycler dropped to 900 mL, and the ultrafiltration volume on the cycler came down to 100 mL. He reports no pain with fill or drain.
What is the next step?
A 28-year-old gentleman, Caucasian descent, comes to clinic for follow up visit. He has been found to have type 1 diabetes mellitus since the age of 12 years of age. His cousin brother has the same disease. He reports no symptoms. He has been using insulin pump using insulin Aspart. He has been monitoring blood sugar using flash glucose monitor and uses carbohydrate count for boluses. He reports infrequent hypoglycemic episodes particularly 2 hours into post lunch, but, manages by himself. He exercises at least at least 60 minutes per day. His vitals recording shows BP of 118/66 mmHg. His BMI is 23.2. System examination is unremarkable.
Value
14.2 gm/L
Sr Sodium
Sr Potassium
4.4 mEq/L
Sr Creatinine
0.6 mg/dL
eGFR using CKD-EPI
136.8 ml/min/1.73m2
Sr Bicarbonate
24 mEq/L
Sr Chloride
Sr Albumin
7.9%
Sr Calcium
Albumin-nil
24-hour urinary protein
76 milligrams/day
What is the MOST LIKELY incorrect statement regarding hyperfiltration stage of Diabetic Kidney Disease in this patient?
The Correct Answer is Option D : eGFR equations like MDRD equation can be used predict hyper filtration.
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 hyper filtration 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.
Direct measurement of GFR is usually required to detect hyperfiltration because estimation equations, such as the Modification of Diet in Renal Disease (MDRD) usually underestimate the true GFR when it is normal or above normal.
Option A : A definite cut off of GFR is lacking. However, renal hyper filtration is typically defined as a GFR of between 120 mL/min and 150 mL/min/1.73m2, or greater than 2 standard deviations above the mean GFR in normal, healthy individuals.
Option B: Hyper filtration in diabetes precedes the onset of albuminuria and/or decline in renal function, and predisposes to progressive nephron damage by increasing glomerular hydraulic pressure
Option C : Hyper filtration per se does not seem to fully explain adverse renal outcome, as the risk for ESRD in transplant donors is very low. However, in type 1 diabetes Rapid GFR decline is associated with renal hyper filtration and impaired GFR and may predict progressive DKD prior to loss of renal function.
Copyright © ABIM Exam World Created On: 10/30/2018 Last Modified: 10/23/2020
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?
Copyright © ABIM Exam World Created On: 09/20/2017 Last Modified: 08/06/2018
Which of the following antihypertensive medications resulted in better blood pressure control and cardiovascular outcomes when combined with an ACE inhibitor?
Copyright © ABIM Exam World Created On: 09/20/2017 Last Modified: 01/28/2021
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.
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 32 year-old male is brought to renal clinic with history of hematuria, oedema feet, and puffiness of face. He gives a history of fever and sore throat a week ago. He also complains of breathlessness on exertion and oliguria. Physical examination shows: Pulse 100/min, BP 150/100 mm Hg, and Temp. 37.4 C. He is pale. He has puffiness of face and oedema feet. Systemic examination-unremarkable. Laboratory examination is as follows:
Hb 10.5 g/d
Hct 34%
Platelet 250,000 mm3
WBC 8,000 mm3
Differential count P 80% L 12% E 6% M 2%
ESR 9.8 mm/h
Urinalysis:
Protein 3000 mg/24 h
Glucose None
RBC 50-60/hpf Dysmorphic
WBC occasional
Leukocyte Esterase Negative
Nitrites Negati
BUN 40 mg/dL
Creatinine 3.9 mg/dL
Sodium 140 mEq/L
Potassium 4.2 mEq/L
Bicarbonate 25.5 mEq/L
S. protein 5.5 g/dl
S. Albumin 2.5 g/dl
Calcium 9.2 mEq/L
Phosphorus 3.2 mg/dL
Glucose 100 mg/dL
Uric Acid 5.3 mg/dL
C 3 Low
C4 normal
HBsAg /HIV Neg
ANA Neg
Kidney Biopsy: Shows enlarged Glomeruli, lobular accentuation, mesangial hypercellularity, endo-capillary proliferation and double contour along the capillary wall. IF shows bright C3 in mesangium and capillary wall with absent immunoglobulin staining.
Electron Microscopy: Suggestive of dense deposits.
What is the BEST treatment option for this patient?
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?
You are about to suspend this exam.
Do you want to suspend this exam?
Do you want to end this exam?
You can always resume the exam from previous tests.