ABIM Qbank Demo

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

		A. Hyperpulsatility of the AV Graft
		B. Reduced pulse augmentation
		C. Increased bleeding and clots
		D. Decreased KT/V
		E. Decreased Blood Flow rate
		E. Surveillance of the graft

Updated:

Explanation:

The correct answer is F

Surveillance of the graft

Explanation:

Intra-graft or venous outflow stenosis – A strong pulse in the AV graft - HYPERPULSATILITY suggests an increase in resistance as occurs with a venous stenotic lesion. The intensity of this pulse is directly proportional to the severity of the stenosis. For this reason, in an AV graft Hyperpulsatility can be considered as an indicator of impending AV graft stenosis.

Arterial stenosis – REDUCED PULSE AUGMENTATION suggests inflow stenosis due to stenosis of the arterial anastomosis or of the feeding artery. Although pulse augmentation is commonly performed, it is less sensitive for the detection of inflow stenosis in AV grafts compared with AV fistulas.

INCREASED BLOOD CLOTS, DECREASED KT/V, and DECREASED BLOOD FLOW RATE are all suggestive of impending AV graft stenosis. Often patients are seen with dilated, collateral veins over the arm and chest wall (very important to examine your hemodialysis patients after taking off their shirts) suggestive of central venous stenosis - The classic physical finding in a patient with a significant central venous stenosis is diffuse upper extremity edema. Subcutaneous collateral veins are frequently evident over the chest. Swelling and collateral veins are caused by generalized venous hypertension of the extremity, which occurs in central, but is rare with peripheral lesions.

SURVEILLANCE does not predict AV Graft stenosis. It is not a sensitive or specific modality to detect the same accurately.

Copyright © ABIM Exam World
Created On: 09/23/2020
Last Modified: 01/28/2021

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

Na 140

Potassium 2.8

Chloride 100

HCO3 26

BUN 15

Creatinine 0.8

Glucose 110

TSH and Cortisol are normal

ACTH elevated

Renin 0.7 (Low)

Aldosterone 48 (elevated)

Urinalysis:

Sodium 240 mEq/D

Potassium 98 mEq/D

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

The most appropriate treatment for this patient is:

		A. Steroids
		B. Spironolactone
		C. Steroids + Spironolactone
		D. Amiloride

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. Chest X ray PA and lateral view
		B. Drain the fluid middle of the day to reduce the dwell time
		C. PD catheter manipulation
		D. Abdominal CT scan with contrast in the dialysate
		E. Switch to hemodialysis
		E. Pleurodesis

Updated:

Explanation:

The correct answer is D

Abdominal CT scan with contrast in the dialysate

Explanation:

Typical ultrafiltration failure from peritoneal membrane failure presents gradually. More frequently, we see an apparent ultrafiltration failure from other reasons.

Catheter malfunction can present with problem with inflow, outflow or both. A kink in the catheter poses problem with inflow and outflow.

Omentum or blood clots clogging the catheter can cause only outflow problem. Fibrin clots, constipation with loaded rectum, and displaced PD catheter also cause outflow obstruction. X ray KUB is very helpful in diagnosing displaced catheter.

FLUID LEAK leak into the abdominal wall causes swelling in the lower abdomen extending down to the scrotum or mons pubis and decrease in the drain volume. Usually this can be treated by temporarily doing low volume PD or transferring to HD for about 6 weeks. Such leaks starting few years after initiating PD usually do not respond to this approach and often requires placement of a new PD catheter.

A patent tunica vaginalis testes will cause UNILATERAL OR BILATERAL SCROTAL SWELLING without much swelling of the abdominal wall sometimes associated with decrease in the drain volume. A CT scan of the abdomen with ‘IV’ contrast into the peritoneal fluid can help in diagnosing the leak into the abdominal wall and scrotal leak. Patent tunica vaginalis testes requires surgery. Generally hemodialysis is not required after the surgery and low volume peritoneal dialysis can be resumed. This patient presents with signs of leak of fluid into the abdominal wall. A chest X ray is not required, so (Choice A) is wrong.

Draining during the middle of the day helps if the membrane is very permeable with very high D/P creatinine ratio on PET. This does not help in abdominal wall leak of dialysate. Therefore, (Choice B) is also wrong.

PD catheter manipulation (Choice C) is wrong because this patient does not have displaced PD catheter from the information given.

(Choice D) is the correct answer. If the clinical presentation is very convincing, most patients are treated with reducing the dialysate volume and if possible keeping the abdomen dry during the day. Sometimes these patients need to be switched to hemodialysis for 4-6 weeks before PD is resumed. Hence temporary switch to HD would be a correct answer, but unqualified switch to HD as is stated in answer E would be a wrong choice. Therefore, (Choice E) is the wrong or less appropriate answer.

ABDOMINAL ADHESIONS cause decrease in the drain volume as well and require surgical treatment with low volume PD or temporary HD after that.

DIAPHRAGMATIC LEAK into the pleural space presents with cough and shortness of breath without peripheral signs of fluid overload few weeks after starting peritoneal dialysis (not the presentation in this patient). Usually, such patients present with right sided pleural effusion clinically and on chest X ray PA and lateral view. These patients can be treated with temporary transfer to HD, pleuridesis and return back to PD 4-6 weeks later. Permanent switch to hemoidialysis without pleurodesis is another option.

TREATMENT OPTIONS OF VARIOUS ABDOMINAL/CHEST PROBLEMS AS MENTIONED ABOVE IN PATIENTS ON PERITONEAL DIALYSIS IS FREQUENTLY TESTED ON BOARDS. PLEASE KNOW THE TREATMENT OPTIONS.

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

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?

		A. Gastric lavage
		B. N-acetylcystiene and activated charcoal
		C. Fomepizole
		D. Fomepizole and Hemodialysis
		E. Obtain serum levels of salycylate, methanol and ethylene glycol levels

Updated:

Explanation:

The correct answer is D

Hemodialysis and fomepizole

Explanation:

While this patient's case may appear to be vague, there are three strong indicators for the most likely diagnosis:

1) This patient has metabolic acidosis with profound Osmolar gap, which is a strong indicator of volatile alcohol related products.

2) Hyperemia of the optic disk (or other ocular symptoms) in addition to profound anion gap should make methanol toxicity a top differential diagnosis.

3) In addition to the serum anion gap, there is a serum Osmolar gap. (Measured Osm – Calculated Osm) where:

Calculated Osmolarity = 2(Na) + BUN/2.8 + Glu/18

***Anytime there is an osmolar gap in metabolic acidosis, your differentials can be narrowed down to volatile alcohol related substances. *** ---------------> IMPORTANT ABIM BOARD POINT

The best treatment for methanol and ethylene glycol is to remove the toxic byproducts from circulation. The definitive therapy is Hemodialysis. Fomepizole is given to block alcohol dehydrogenase, thereby stopping the formation of toxic byproducts. However, it does not remove them from circulation, only dialysis can do this.

(Choice A) Gastric lavage is almost never the correct answer, especially with ingestion of an unknown substance. Caustic substances can cause further damage on the way out with the use of gastric lavage. Esophageal perforation is potentially a fatal risk.

(Choice B) N-acetyl cystiene is the treatment for acetaminophen toxicity however timing is important and drug levels should be drawn first to determine the need for treatment. If ingestion occurred more than 24 hours earlier, treatment has no effect and is therefore not given.

(Choice C, D) Refer to the explanation section above.

(Choice E) When suspicion for methanol poisoning is high, treatment should not wait for diagnosis confirmation. The presence of ocular involvement is an ominous sign, and the risk of blindness is increased. The benefits outweigh the risk of treating before confirming diagnosis in this case.

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

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?

		A. Mycophenolate and steroid
		B. Mycophenolate, tacrolimus and steroids
		C. Rituximab
		D. I.V Immunoglobulins
		E. Plasma exchange

Updated:

Explanation:

The correct answer is B

Mycophenolate, tacrolimus and steroids

Explanation:

This patient had membranous lupus being treated with Euro-Lupus regime. Activity in the urine with a positive ANA and dsDNA and low C3, C4 suggests activity of the disease. The biopsy is showing active lupus nephritis combined with features of class IV & V diffuse proliferative GN. Patients with both DPGN and membranous lesions are more likely to be resistant to standard induction regimens with cyclophosphamide or MMF with steroids. In these patients, combined treatment with MMF and tacrolimus is recommended. This was suggested by Bao H. et al in a small, short term prospective trial in which 40 patients with diffuse proliferative plus membranous lupus nephritis were randomly assigned to induction therapy with MMF (0.75g to 1g/d) and tacrolimus (3-4 mg/d) or intravenous cyclophosphamide alone .All patients received steroids. At nine months there was significantly higher rate of complete remission in patients treated with MMF and tacrolimus as compared to cyclophosphamide (65% versus 15%).

(Choice A) Mycophenolate and steroids can be used in patients who have received cyclophosphamide and are resistant to it.

(Choice C and D) Rituximab and I.V. Immunoglobulins can be used in patients with lupus nephritis who have failed to respond to cyclophosphamide, MMF and steroids.

(Choice E) Plasma exchange is recommended in patients with SLE and (TTP).

KDIGO Clinical Practice Guidelines for Glomerulonephritis recommends the following treatment for resistant lupus nephritis:

Treatment of resistant disease 12.9.1: In patients with worsening S. Cr and/or proteinuria after completing one of the initial treatment regimens, consider performing a repeat kidney biopsy to distinguish active LN from scarring. (Not Graded) 12.9.2: Treat patients with worsening S. Cr and/or proteinuria who continue to have active LN on biopsy with one of the alternative initial treatment regimens. If patient has received cyclophosphamide use MMF and if patient has received MMF use cyclophosphamide (Not Graded) 12.9.3

KDIGO suggests that non -responders who have failed more than one of the recommended initial regimens (cyclophosphamide, MMF or CNI) may be considered for treatment with rituximab, IV Immunoglobulins, or CNIs. (2D).

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

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.

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% 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 ?

		A. Diabetic Kidney Disease previously called as diabetic nephropathy can be diagnosed clinically with renal biopsy only.
		B. Presence of microalbuminuria is adequate for clinical diagnosis of Diabetic Kidney Disease.
		C. Presence of hematuria without non-diabetic kidney disease is impossible in Diabetic Kidney Disease as diabetic kidney disease is a non-proliferative glomerular disease.
		D. Family history of Diabetic Kidney Disease is associated with renal involvement in Diabetes.

Updated:

Explanation:

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.

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?

		A. Three-year graft survival is inferior to blood group compatible transplants.
		B. The infectious and bleeding complications post ABOI kidney transplant are the same as blood matched kidney transplant.
		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.
		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.

Updated:

Explanation:

Correct answer: Option D: C4d staining on protocol biopsies is common feature and does not necessarily mean an antibody mediated rejection process.

Explanation:

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 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?

		A. Acute poststreptococcal glomerular nephritis
		B. Diffuse proliferative lupus nephritis
		C. Dense deposit disease
		D. C3 glomerulopathy
		E.

Updated:

Explanation:

The correct answer is D

C3 glomerulopathy

Explanation:

This patient has proteinuria, microscopic hematuria, hypertension and edema suggestive of acute nephritis of 2 months duration. The classic prototype of acute nephritis is acute post streptococcal glomerulonephritis. Typically in the acute post infective glomerular nephritis, complement levels normalize in 6 weeks and generally proteinuria and microhematuria resolve in approximately 6 weeks. Hence (Choice A) is wrong. This patient has hypocomplementemia and features of acute nephritis for 2 months suggesting that we should look for other causes of acute nephritis.

Acute nephritis with low complement levels:

Post-infectious glomerulonephritis

Lupus nephritis

Membranoproliferative glomerular nephritis

Mixed cryoglobulinemia

C3 Nephropathy

Acute nephritis with normal complement levels:

IgA nephropathy

Thin basement membrane disease

Hereditary nephritis

HSP

Mesangial proliferative glomerulonephritis

Lupus nephritis

Membranoproliferative glomerular nephritis

Mixed cryoglobulinemia

Dense deposit disease

This patient is a male and ANA is negative. Lupus is mainly a disease affecting young women in third and fourth decade and most of them are ANA positive. A variety of glomerular pathologies are described, but immunofluorescence typically shows ‘full house’ pattern with positive IgG, IgM, IgA and C3. ANA negativity and not having the IF picture showing full house to suggest lupus nephritis makes lupus nephritis (Choice B) unlikely.

Dense deposit disease is type II MPGN and it mainly affects children and young adults. In the majority of patients there is circulating C3 nephritic factor. Immunofluorescence microscopy demonstrates C3 deposits, and EM shows characteristic sausage-shaped, wavy deposits along the glomerular basement membranes (GBM) and mesangium. Lack of typical EM appearance makes dense deposit disease (Choice C) unlikely.

C3 Glomerulopathy is a morphologic variant of MPGN type I. In “C3 glomerulopathy”, different light microscopy pathologies such as mesangioproliferative, membranoproliferative glomerulonephritis, diffuse proliferative glomerulonephritis, crescentic GN and Sclerosing GN has been described. C3 level is usually low and C4 level is normal. In Sclerosing disease, C3 level can also be normal. The distinct feature of this is that IF shows exclusively C3 deposits, without any immunoglobulins. EM does not show sausage shaped intra-membranous deposits. Hence, the correct choice is (Choice D).

C3 glomerulopathy can present with varying degrees of proteinuria, azotemia and can advance to ESRD. It can recur after transplantation.

Educational Objective:

C3 glomerulopathy can present with varying degrees of proteinuria, azotemia and can advance to ESRD. It can recur after transplantation.

C3 glomerulopathy is a morphologic variant of MPGN type I. The distinct feature of this is that IF shows exclusively C3 deposits, without any immunoglobulins. EM does not show sausage shaped intra-membranous deposits.

IMPORTANT BOARD EXAM ADVICE:

1. Differentiate between DDD and C3GN

2. Know the glomerulonephritis with low and normal complement levels.

3. BOARD QUESTIONS will be asked on DDD and C3GN, so know it well.