A 15 year-old boy is brought to the ER by his foster mother who states that when she got home from work she noticed he was acting very strange. He had slurred speech and seemed confused. He appeared to be very uncoordinated and she was not sure if he fell or hit his head. She states that he is somewhat a troubled boy but doesn’t know much about his history as he has been in and out of the foster care system out of state. On physical exam, he is tachycardic and has tachypnoea. Pupils are dilated, but there is no nystagmus. A fundoscopic exam shows hyperemia of the optic disk. He is relatively uncooperative but not aggressive or hostile. When asked about suicidal thoughts he responds only with inaudible mumbling. His foster mother left for work 10 hours prior and assumed he left for school. She is not sure when these symptoms began or what may have initiated them. P is 105/ min, BP is 140/90 mm Hg, RR is 28/min, and T is 97.1 F. Laboratory examination is as follows:
Na 135 mEq/L
K 5.0 mEq/L
CL 105 mEq/L
BUN 19 mg/dL
Cr 1.3 mg/dL
HCO3 8 mEq/L
Glucose 100 mg/dL
pH 7.3
pO2 90 mmHg
pCO2 22 mmHg
Measured serum osmolarity 320 mmol/L
What is the next step in management?
Copyright © ABIM Exam World Created On: 09/13/2017 Last Modified: 12/30/2017
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 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 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
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
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?
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
An 18 year-old male is brought to the renal clinic for evaluation of hypertension. There is no history of edema of the feet, puffiness of the face, hematuria, oliguria ,or recurrent urinary tract infections. He is an active football player, but lately he complains of weakness and muscle cramps. His blood pressure for the last 3-4 years has always been borderline high and during this visit was as noted below.
Physical examination shows: Pulse 100/min, all peripheral pulsations are well felt. BP 150/100 mm Hg, Temp. 37.4 degrees C. He is pale. His growth is stunted. His cognitive function is normal and no focal neurological deficits are noted. Other systems are unremarkable. Laboratory examination is as follows:
Hemoglobin 13.5 g/dL
Hematocrit 42%
White Blood Cells 8,000 mm3
Protein 100 mg/24 h
Red Blood Cells None
White Blood Cells None
Chemistry:
BUN 13.5 mg/dL
Creatinine 0.9 mg/dL
Potassium 5.8 mEq/L
Bicarbonate 18.5 mEq/L
Chloride 112 mEq/l
Phosphorus 3.2 mg/dL
Aldosterone 5 ng/mL
PRA <1.0ng/dl/hr
HbA1C 5.30%
S. Osmolality 282 mOsmol
ESR 9.8 mm/h
ABG:
pH 7.25
PCO2 32 mm Hg
HCO3 16 mEq/L
PO2 90 mm Hg
USG Normal size kidneys, no hydronephrosis
Considering the history and the laboratory findings, which of the following is most likely the cause of hypertension in this patient?
Copyright © ABIM Exam World Created On: 09/20/2017 Last Modified: 01/25/2021
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 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.
13.2 gm/L
7.8 X 103/cubic mm
136 mEq/L
4.2 mEq/L
153.1 ml/min/1.73m2
8.2%
86 milligrams/day
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 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?
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 :
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
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
50-year-old female patient whos group B is being evaluated for kidney transplant surgery. She had ESRD secondary to analgesic nephropathy and is on hemodialysis for last 5 years. She has had multiple sensitization events in the form of 3 pregnancies and several blood transfusions. Her current calculated PRA against class I antigen is 97% and against class II antigen is 99%. She has been enrolled in the national highly sensitized recipient program.
Her husband who is blood group matched came forward as a potential kidney donor but she had positive Flow B and T Cell Cross match against him. Single antigen bead assay demonstrated that she has donor specific antibodies against class II across DQB*15 and DPB*14. This transplant did not materialize as patient declined desensitization protocol. Now her younger brother comes forward as a potential donor. He is blood group A and the flow B and T cell cross match is negative with no demonstrable donor specific antibodies against this donor.Patient wants to know more about ABO incompatible transplant.
Which of the following statements about the ABO incompatible transplant is correct?
Correct answer: Option D: C4d staining on protocol biopsies is common feature and does not necessarily mean an antibody mediated rejection process.
Choice A: Three-year graft survival is inferior to blood group compatible transplants is incorrect A comprehensive database analysis of 1420 ABOI living donor (LD) kidney transplants performed in 101 centers from 2005 to 2012 compared graft and patient survival to a matched cohort of ABO-compatible transplant recipients. Three-year graft and patient survival were ultimately identical. 1
Choice B: The infectious and bleeding complications post ABOI kidney transplant as same as blood matched kidney transplant is also incorrect. Using USRDS and Medicare data from 2000–2007, 119 ABOI (non-A2 donor) transplant recipients were identified. Compared with ABO-compatible recipients, the risks of infectious and hemorrhagic complications were significantly higher, with a 2.2-fold higher risk of pneumonia, a 3.5-fold higher risk of wound infections, a 56% higher risk of pyelonephritis, and a nearly 2- fold higher risk of hemorrhage 2
Choice C: All patients undergoing ABOI transplant need to undergo desensitization using IVIg, Plasma exchange, Rituximab irrespective of their donor/recipient pair Anti ABO titers for optimal outcomes is also an incorrect answer. Historically, ABOI transplantation has been successful when performed after desensitization with plasmapheresis, intravenous Ig (IVIG), rituximab, and/or splenectomy to achieve ABO IgG antibody titers 1:4. A recent publication demonstrated that these intensified treatments might not be necessary in donor/recipient pairs who have low-moderate titer ABO incompatibility 3
Choice D: C4d staining on protocol biopsies is common feature and does not necessarily mean an antibody mediated rejection process in the absence of allograft dysfunction is the correct answer C4d staining is not an uncommon feature seen in the protocol biopsies done in ABOI kidney transplant recipients. In the absence of allograft dysfunction, the C4d staining has no clinical relevance and is just a part of the graft accommodation.
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)
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:
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?
Copyright © ABIM Exam World Created On: 09/14/2017 Last Modified: 08/06/2018
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
Protein 3000 mg/24 h
RBC 50-60/hpf Dysmorphic
WBC occasional
Nitrites Negati
BUN 40 mg/dL
Potassium 4.2 mEq/L
Bicarbonate 25.5 mEq/L
S. protein 5.5 g/dl
S. Albumin 2.5 g/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?
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
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)
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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