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TUTOR - CKD / ESRD / MBD

Test Id: 1869464d645156f064
QId: 165258

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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?

		A. Paricalcitol treatment reduced LV mass
		B. Paricalcitol treatment preserved LV ejection fraction
		C. Paricalcitol treatment improved pulse wave velocity and arterial stiffness
		D. Paricalcitol treatment improved blood pressure control
		E. Paricalcitol treatment significantly reduced PTH and alkaline phosphatase

Explanation:

The correct answer is E

Paricalcitol treatment significantly reduced PTH and alkaline phosphatase

Explanation:

Vitamin D Rx DOES NOT reduce LV mass OR LV ejection fraction OR arterial stiffness

Vitamin D seems to protect against cardiovascular disease, but the reported effects of vitamin D on patient outcomes in CKD are controversial.

OPERA trial was a prospective, double blind, randomized, placebo-controlled trial to determine whether oral activated vitamin D reduces left ventricular (LV) mass in patients with stages 3-5 CKD with LV hypertrophy.

Subjects with echocardiographic criteria of LV hypertrophy were randomly assigned to receive either oral paricalcitol (1 ?g) one time daily (n=30) or matching placebo (n=30) for 52 weeks.

The primary end point was change in LV mass index over 52 weeks, which was measured by cardiac magnetic resonance imaging. Secondary end points included changes in LV volume, echocardiographic measures of systolic and diastolic function, biochemical parameters of mineral bone disease, and measures of renal function.

Change in LV mass index did not differ significantly between groups (median [interquartile range], -2.59 [-6.13 to 0.32] g/m(2) with paricalcitol versus -4.85 [-9.89 to 1.10] g/m(2) with placebo).

Changes in LV volume, ejection fraction, and tissue Doppler-derived measures of early diastolic and systolic mitral annular velocities, and ratio of early mitral inflow velocity to early diastolic mitral annular velocity did not differ between the groups.

Paricalcitol treatment significantly reduced intact parathyroid hormone (P<0.001) and alkaline phosphatase (P=0.001) levels as well as the number of cardiovascular-related hospitalizations compared with placebo.

52 weeks of treatment with oral paricalcitol (1 ?g one time daily) significantly improved secondary hyperparathyroidism but did not alter measures of LV structure and function in patients with severe CKD and ESRD.

OPERA and PRIMO are two recent randomized clinical trials in patients with CKD, which evaluated paricalcitol for slowing the progression of left ventricular mass. Both these trials were found to have negative results.

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TUTOR - Hypertension

Test Id: 1869464d645156f064
QId: 165243

2 of 16

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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?

		A. Type 4 RTA
		B. Pseudo-hypo-aldosteronism Type 1
		C. Gordon's syndrome
		D. Diarrhea

Explanation:

The correct answer is B

Pseudo hypo-aldosteronism type 1

Explanation:

This patient has hyponatremia with high urinary sodium. High serum potassium, low urinary potassium, and normal adrenal function. The serum aldosterone level is high, suggesting resistance to aldosterone action of target organ. These findings are characteristic of Pseudohypo aldosteronism type1 (PHA Type1)

PHA type1 is a rare hereditary disorder, characterized by generalized resistance to the action of aldosterone. It presents with

1. Salt wasting

2. Hypovolemia

3. Normotension

4. Metabolic acidosis

5. Hyperkalemia

6. High Renin and Aldosterone.

NEPHROLOGY BOARD EXAM TAKERS REMEMBER THESE 6 POINTS FOR PHA TYPE 1

These are two different modes of inheritance:

1] Autosomal recessive.

2] Autosomal dominant.

Autosomal recessive affects the epithelial sodium channel and other target organs like kidney, colon, and sweat gland. There is a down regulation of the sodium channels and decreased sodium transport.

Autosomal dominant or sporadic form is due to heterozygous mutations in the NR3C2 gene coding for mineralocorticoid receptor. This is milder form than autosomal recessive disease in which only kidney is affected. The disease often improves with age.

Treatment consists of high salt diet. This prevents volume depletion and by enhancing sodium delivery to the distal tubules, potassium exertion increases, thereby bringing down the serum potassium.

High dose Fludrocortisone (1 to 2 mg/day ), or Carbenoxolone is indicated if high salt intake is ineffective or not tolerated.

(Choice A) Type IV RTA will have low aldesterone and low renin level. Therefore, that is not the likely answer.

(Choice D) Diarrhea will have metabolic acidosis with hypokalemia and Net urine charge will be negative. This patient has positive Net urine charge with hyperkalemia which rules out diarrhea as a cause.

(Choice C) = PHA TYPE 2 (Pseudohypoaldosteronism type 2) OR = Gordon’s syndrome is characterized by:

1. Hypertension

2. Hyperkalaemia

3. Metabolic acidosis

4. Low plasma Renin and Aldosterone. This is due to mutations in WNK kinases 1 and 4. These mutations result in increased chloride reabsorption with sodium retention thereby resulting in hypertension.

NEPHROLOGY BOARD EXAM TAKERS REMEMBER THESE 4 POINTS FOR PHA TYPE 2 or GORDON's SYNDROME

IF YOU KNOW THESE 10 POINTS OF PSEUDOHYPOALDOSTERONISM TYPE 1 & 2 THAN YOU CAN ANSWER ALL QUESTIONS ON PHA 1, 2 AND GORDON'S SYNDROME WHICH ARE GOING TO BE ASKED FOR SURE ON THE BOARDS.

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TUTOR - CKD / ESRD / MBD

Test Id: 1869464d645156f064
QId: 165260

3 of 16

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You are rounding on your patients in the dialysis unit and seeing a 65-year-old gentleman with ESRD due to chronic interstitial disease. He also has a history of diet-controlled diabetes mellitus and hypertension. His other past medical history is significant for dyslipidemia, coronary artery disease, hypothyroidism, gout and depression. He has been hospitalized in the recent past for swelling and pain of his right great toe. He was seen by the foot doctor, a scan was done and eventually the great toe had to be amputated. He has been on hemodialysis 3 times a week. His weekly Kt/V is 1.9. You are conducting the monthly blood work review for this patient. You note that his hemoglobin has been persistently low for past few monthly blood draws. He is currently on 100 mcg of Darbepoetin weekly on dialysis. On enquiry there is no history of blood loss in the form of hematemesis, melena, hematochezia or hemoptysis. His active medication list includes Losartan, Atorvastatin, Calcitriol, multivitamin supplements, paroxetine, allopurinol, aspirin.

His pertinent blood work is as follows:

Test	Result
WBC	4500 cells /cumm
Hemoglobin	8.2 g/dL
Platelet count	450 thousand /cumm
Reticulocyte count	Normal
Iron	55 (range 50-150)
Total iron binding capacity	250 g/dl (range 250-310)
Transferrin saturation	20%
Ferritin	1400 ng/ml (range 20-235)
Haptoglobin	400 mg/dl (range 83-267)
Lactate dehydrogenase	240 U/L (range 80-225)
Total bilirubin	1.0 mg/dl
Folate	7 ng/ml (range 1.8-9.0)
B12	500 pg/ml (range 200-800)
Peripheral blood smear.	Normal RBC morphology, few burr cells.

Which of the following is true about this patient’s anemia?

	Erythropoietin deficiency. Check EPO levels.
	ESRD patients tend to have low Hepcidin production due to renal failure. This contributes to anemia.
	This patient has chronically inflamed state and this is contributing to his anemia.
	Patient has developed pure red cell aplasia.
	Patient is under dialysed. Start daily dialysis to overcome EPO resistance.

Explanation:

Correct Answer: Option C: This patient has chronically inflamed state which is contributing to his anemia.

Explanation:

10-15% of patients who have been receiving erythrocyte estimating agents (ESA) develop resistance. There are multiple reasons why ESRD patients develop resistance.

ESA resistance occurs due to the following reasons:

Iron deficiency.
Chronic inflammation.
Under-dialysis.
Hemolysis.
Folate and B12 deficiency.
Chronic blood loss.
Anti EPO antibodies.
Pure red cell aplasia.
Failed chronic renal allograft.
ACEI/ARB.
Aluminum overload.
Hyperparathyroidism.
Hematological disorders or malignancy.

Option A: Incorrect option. ESRD is associated with erythropoietin deficiency. Patient has been initiated on ESA already. There is no point in measuring EPO levels. There is no evidence of measuring EPO levels in management of anemia in CKD.

Option B: Incorrect option. ESRD is an inflamed state. In inflammatory milieu there is increased production of Hepcidin. The hepatic iron-regulatory hormone Hepcidin and its receptor, the cellular iron exporter Ferroportin, constitute a feedback-regulated mechanism that maintains adequate plasma concentrations of iron-transferrin for erythropoiesis and other functions, ensures sufficient iron stores, and avoids iron toxicity. In chronic kidney disease, inflammation and impaired renal clearance increases plasma hepcidin, inhibiting duodenal iron absorption and sequestering iron in macrophages. These effects of hepcidin can cause systemic iron deficiency, decreased availability of iron for erythropoiesis, and resistance to endogenous and exogenous erythropoietin.

Choice C: Correct option. Refer explanation for option B. He had pain, swelling of his right great toe, a foot doctor sees him, a bone scan is done and subsequently the amputation. All suggestive of an infective etiology probably osteomyelitis.There is a temporal relationship between patients’ anemia and underlying chronic inflammatory state.

The high ferritin is also suggestive of inflamed state.

Choice D: Incorrect option. Pure red cell aplasia, a form of severe ESA hypo-responsiveness mediated by anti-erythropoietin antibodies, was first reported with certain formulations of Epoetin alfa but has now been reported with all commercially available forms of ESA. This syndrome presents with rapid onset of severe anemia (hemoglobin <7 g/dl), severe reticulocytopenia (reticulocyte count <10,000/?l) and marked elevations in serum ferritin level (>1000 ng/ml) and transferrin saturation (>70%) resulting from low iron utilization. Pure red cell aplasia is unlikely given the absence of characteristic laboratory findings. Moreover, the patient did not receive Epoetin alfa.

Choice E: Incorrect option. Under-dialysis leads to anemia due the same mechanism mentioned earlier in option B. Under-dialysis worsens the uremic milieu which in turn leads to inflammatory state. This leads to anemia. Patient in this clinical vignette has been dialysed appropriately. His weekly Kt/V is 1.9, which is above the target goal of 1.7

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TUTOR - CKD / ESRD / MBD

Test Id: 1869464d645156f064
QId: 1673177

4 of 16

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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

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.

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TUTOR - Glomerulonephritis

Test Id: 1869464d645156f064
QId: 165246

5 of 16

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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. Plasma exchange + Rituximab
		B. Rituximab
		C. Eculuzimab
		D. Cyclophosphamide + Steroids

Explanation:

The correct answer is C

Eculuzimab

Explanation:

This patient has nephritic-nephrotic picture with low C3. The Kidney biopsy along with clinical presentation is suggestive of MPGN. Negative Immunoglobulins along with positive C3 staining narrows it down to DDD (DENSE DEPOSIT DISEASE) or C3-GN (C3-GN GLOMERULONEPHRITIS)

DDD or Dense deposit disease is best treated with Eculuzimab.

Rituximab has not been found to be useful in DDD or C3-GN.

ECULUZIMAB : has been shown to be useful in:

1. DDD

2. Atypical HUS – used along with plasma exchange. If using Eculuzimab give meningococcal vaccine or give penicillin till the vaccine becomes effective.

However, (additional information not pertaining to this question)

RITUXIMAB : has been shown to be useful in:

1. ANCA vasculitis (can be used in induction or relapse – RAVE TRIAL)

2. Wegeners

3. HCV cryoglobulinemia

TTP

***** TREATMENT OPTIONS IN GLOMERULONEPHRITIS WITH RITUXIMAB AND ECULUZIMAB ARE FREQUENTLY TESTED CONCEPTS IN NEPHROLOGY BOARD EXAMS. PLEASE REVIEW THESE IN DETAIL.*****

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TUTOR - CKD / ESRD / MBD

Test Id: 1869464d645156f064
QId: 167339

6 of 16

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

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

Explanation:

The correct answer is F

Surveillance of the graft

Explanation:

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

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TUTOR - Acute Kidney Injury / ICU Nephrology

Test Id: 1869464d645156f064
QId: 165256

7 of 16

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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?

		A. Indinavir
		B. Tumor lysis syndrome
		C. Antifreeze ingestion
		D. Acyclovir
		E. IV TMP/SMX

Explanation:

The correct answer is D

Acyclovir

Explanation:

This patient has a characteristic lesion of herpes zoster on his neck. The vesicles are 2-3 mm in size with erythematous base. They are in different stages of development. Herpes zoster is commonly seen in elderly and immunocompromised. This patient is 30 year old and immunocompromised (HIV positive with AIDS). The treatment of choice for herpes zoster in immunocompromised patient is IV acyclovir. High dose Acyclovir is one of the causes of crystal-induced nephropathy. The crystals are needle-shaped.

Indinavir (Choice A), a protease inhibitor, is a common cause of nephrolithiasis in HIV patients. Patients would often present with flank pain. Urinalysis would show hematuria and needle shaped crystals. This patient, however, had normal serum chemistry on presentation. Following two days of IV medication (acyclovir) his serum chemistry showed elevated creatinine suggesting acyclovir as the most likely cause.

Tumor lysis syndrome (Choice B) occurs in the setting of chemotherapy for lymphoma. It leads to the formation of uric acid crystals which are also needle shaped. This patient has no such presentation.

Patients with Anti-freeze ingestion (Choice C) present with metabolic acidosis with an elevated anion gap. The initial test of urinalysis shows envelope-shaped oxalate crystals.

Trimethoprim-sulfamethoxazole (TMP/SMX) (Choice E) has sulfonamide in it. Sulfonamide also leads to crystal-induced nephropathy. The crystals are often dumb-bell shaped.

Educational Objective:

Drugs causing Crystal-induced nephropathy:

ACYCLOVIR --- Needle shaped crystals

INDINAVIR --- Needle shaped crystals

SULPHONAMIDE --- Dumbell shaped crystals

CALCIUM OXALLATE (Antifreeze) --- Envelope shaped crystal

CALCIUM PO4---- Coffin shaped crystals

URIC ACID --- Hexagonal crystals

CYSTIENE --- Hexagonal crystals

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TUTOR - Hypertension

Test Id: 1869464d645156f064
QId: 165215

8 of 16

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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%

Platelet Count 150,000 mm3

White Blood Cells 8,000 mm3

Urinalysis:

Protein 100 mg/24 h

Glucose None

Red Blood Cells None

White Blood Cells None

Leukocyte Esterase Negative

Nitrites Negative

Chemistry:

BUN 13.5 mg/dL

Creatinine 0.9 mg/dL

Sodium 140 mEq/L

Potassium 5.8 mEq/L

Bicarbonate 18.5 mEq/L

Chloride 112 mEq/l

Calcium 9.2 mEq/L

Phosphorus 3.2 mg/dL

Aldosterone 5 ng/mL

PRA <1.0ng/dl/hr

Glucose 100 mg/dL

HbA1C 5.30%

S. Osmolality 282 mOsmol

Uric Acid 5.3 mg/dL

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?

		A. Liddle's Syndrome
		B. Gordon's Syndrome
		C. Congenital adrenal hyperplasia
		D. Glucocorticoid-remediable aldosteronism
		E. Mineralocorticoid receptor activating mutation

Explanation:

The correct answer is B

Gordon’s syndrome

Explanation:

Gordon’s syndrome - Young male with hypertension, hyperkalemia, hyperchloremic metabolic acidosis, normal renal function, low rennin, and low aldosterone is highly characteristic of Gordon’s syndrome. This syndrome is also known as pseudohypoaldosteronism type II. Recently it has been reported that Gordon’s syndrome is linked to chromosomes 1, 12, and 17. Hyperkalemia and hypertension in Gordon’s syndrome are caused by abnormalities in WNK kinases, proteins that are localized to the distal nephron and affect the thiazide-sensitive Na-Cl Cotransporter. Mutations affecting either WNK4 or WNK1 result in increased chloride reabsorption in the distal nephron, thereby reducing lumen electronegativity and lowering the force for potassium secretion. These mutations also result in decreased expression of the potassium channels through which potassium enters the collecting duct. Thus, mutant WNK4 increases sodium chloride reabsorption in the distal tubule and decreases potassium secretion in the collecting tubule resulting in sodium retention and decreased potassium excretion resulting in hypertension, hyperkalemia, and metabolic acidosis. The volume expansion leads to suppression of rennin and aldosterone.

(Choice A) Liddle’s syndrome presents as hypertension in childhood. It is usually resistant to standard antihypertensive drugs. This is due to gain of function mutation at chromosome 16 affecting the beta or gamma subunit of ENaC channel in collecting duct of the nephron. This results in sodium retention and volume expansion causing hypertension and hypokalemia. The volume expansion leads to suppression of rennin and aldosterone. These patients will have hypertension, hypokalemia, metabolic alkalosis, low rennin and low aldosterone.

(Choice C) Congenital adrenal hyperplasia presents in childhood with hypertension and virilization in girls and precocious puberty in boys. The other features include primary amenorrhea, delayed sexual maturation, ambiguous genitalia, with clitoral enlargement in girls. The 11 beta hyroxylase (CYP11B1) and (17 alpha hydroxylase (CYP17) deficiencies lead to excess deoxycoticosterone which leads to hypertension through a mineralocorticoid action. Biochemically it is characterized by metabolic alkalosis, low rennin and low aldosterone.

(Choice D) Glucocorticoid-remediable aldosteronism (GRA) is also known as familial hyperaldosteronism type I. In this disorder there is a chimeric gene formed from portions of the 11-beta-hydroxylase gene (CYP11B2) and the aldosterone synthase gene (CYP11B2). Patients with GRA have ectopic aldosterone synthesis occurring in the zona - fasciculata under the direct influence of ACTH rather than the renin. GRA presents with hypertension, hypokalemia, metabolic alkalosis, low rennin and high aldosterone. GRA resembles a primary hyperladosterone state with excessive urinary potassium loss. Look for a clue of family history of CVA or brain haemorrhage in the stem of the question.

(Choice E) Mineralocorticoid receptor activating mutation is a very rare autosomal dominant disorder. The mutation lies in the mineralocorticoid receptor, which causes it to be activated by steroid lacing 21 –hyroxyl groups, such as progesterone and spironolactone. Both normally antagonize the receptor but have opposite effect on this mutant receptor. It usually present as early onset hypertension in females. It may get accelerated during pregnancy due to elevated levels of progesterone. Biochemically it is characterized by hypokalemia, metabolic alkalosis low renin and low aldosterone.

Educational objective:

IF YOU KNOW THESE 5 POINTS FOR THESE 5-6 SYNDROMES YOU CAN ANSWER ALL NEPHROLOGY BOARD QUESTIONS ASKED ON THESE SYNDROMES:

Blood pressure - Normotension or hypertension

Potassium - Hyperkalemia or hypokalemia

Acid-Base - Acidosis or alkalosis

Renin - Low or High

Aldosterone - Low or High

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TUTOR - PHARMACOLOGY

Test Id: 1869464d645156f064
QId: 16521

9 of 16

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As per the JNC VIII committee recommendation, for individuals that are part of the African American population, including those with diabetes, the initial treatment should include a thiazide type diuretic or calcium channel blocker (CCB).

Which of the following thiazide type diuretic is preferred as the initial antihypertensive therapy?

		A. Hydrochlorthiazide
		B. Chlorthalidone
		C. Indapamide
		D. Metalazone
		E. Polythiazide

Explanation:

The correct answer is B

Chlothalidone

Explanation:

• Chlorthalidone at the same dose is approximately 1.5 to 2 times as potent as hydrochlorothiazide.

• Chlothalidone has a longer duration action than hydrochlorothiazide.

• There are No randomized clinical trials that directly compare outcomes in hypertensive patients treated with hydrochlorothiazide versus chlorthalidone. A multiple treatment (network) meta-analysis of nine trials including 50,946 patients was conducted in which hydrochlorothiazide and chlorthalidone were indirectly compared by evaluating their efficacy against common comparative drugs (ACE inhibitors were compared with hydrochlorothiazide in ANBP2 trial and with chlorthalidone in ALLHAT trial). The major findings of this meta-analysis showed that chlorthalidone significantly reduced the risk of cardiovascular events compared to hydrochlorothiazide (relative risk 0.79, 95% CI 0.72 to 0.88) and heart failure (relative risk 0.77, 95% CI 0.61 to 0.98). The authors calculated that 27 patients would need to be treated with chlorthalidone instead of hydrochlorothiazide over five years to prevent one cardiovascular event. Chlorthalidone remained superior to hydrochlorothiazide even after the meta-analysis was controlled for achieved office systolic blood pressure (relative risk for cardiovascular events 0.82, 95% CI 0.70 to 0.97). This finding may reflect the longer duration of action and lower nocturnal blood pressure associated with chlorthalidone.

• Multiple Risk Factor Intervention Trial (MRFIT) - Men Hypertensive 2392 were treated with chlorthalidone and 4049 were treated with hydrochlorothiazide. During six years of follow-up, cardiovascular events (defined as myocardial infarction, stroke, coronary artery bypass surgery, heart failure, left ventricular hypertrophy, peripheral artery disease, or angina) were significantly less common with chlorthalidone compared with hydrochlorothiazide (hazard ratio 0.79, 95% CI 0.68 to 0.92). Through the course of the study, systolic blood pressure and LDL cholesterol levels were also lower with chlorthalidone compared with hydrochlorothiazide.

• Indapamide - is a thiazide like diuretic and has a half-life of 14-16 hours. This drug has been used in HYVET trial alone or in combination with perindropril in treatment of hypertension in patients more than 80 years old. Study showed 30% reduction in stroke, 39% reduction in the rate of death .21%in death from any cause, 23%reduction in CV death and 64%reduction in the rate of heart failure. The trial has shown careful BP lowering in very elderly is beneficial. Indapamide is not preferred over chlorthalidone.

• Metalazone - There are many studies with metalazone available. An important additional property is its effectiveness as a diuretic at lower GFR value. The duration of action is about 24 hours.

It is not preferred over chlorthalidone.

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TUTOR - Kidney Transplantation

Test Id: 1869464d645156f064
QId: 167345

10 of 16

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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. Interstitial Fibrosis
		B. Tubular atrophy
		C. Endothelial cell swelling
		D. Glomerular thrombin deposits
		E. Glomerular basement membrane thickening
		E. Double contours of the GB

Explanation:

The correct answer is D

Glomerular thrombin deposits

Explanation:

In a patient with suspected cyclosporine nephrotoxicity, the renal biopsy reveals an obliterative arteriolopathy (which is classically seen in afferent renal arterioles) suggesting primary endothelial damage and subsequently endothelial cell swelling which may persist for months in a patient with elevated cyclosporine blood levels. This is also associated with thickened glomerular basement membrane and double contour pattern. In fact according to BANF thickened glomerular basement membrane and double contour pattern is most suggestive of chronic allograft nephropathy (CAN) also called as TRANSPLANT GLOMERULOPATHY.

The other renal biopsy findings of cyclosporine nephrotoxicity include ischemic collapse or scarring of the glomeruli, vacuolization of the tubules, FSGS, and focal areas of tubular atrophy and interstitial fibrosis (producing a picture of “ZEBRA” or "STRIPED" fibrosis) These changes are seen with both low-dose and higher-dose cyclosporine therapy, although they seem to co-relate earlier with higher doses.

(THE ABOVE PICTURE IN THE UPPER HALF SHOWS TUBULAR ATROPHY APPEARING DARK AND REDDISH ALTERNATING WITH LIGHT BLUE AREAS OF INTERSTITIAL FIBROSIS GIVING A "STRIPED" OR "ZEBRA" APPEARANCE)

THE PICTURE BELOW SHOWS TUBULAR ATROPHY, VACUOLIZATION OF THE TUBULES AND ISCHEMIC CHANGES:

Mild arteriolar hyalinosis at six months appears to be associated with high doses of cyclosporine and was reversible. However, after more than a year irreversible severe arteriolar hyalinosis and glomerulosclerosis were observed, despite decreased doses and trough levels of cyclosporine.

Glomerular thrombin deposits are typically seen in patients with Lupus, anti phospholipid syndromes and other vasculitides. It is typically not seen in cyclosporine nephrotoxicity.

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TUTOR - Hypertension

Test Id: 1869464d645156f064
QId: 165212

11 of 16

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The ACCOMPLISH trial is the first major trial addressing the issue of combination therapy in 11,506 patients who were at high cardiovascular risk. The goal blood pressure was less than 130/80 mm Hg in the patients with diabetes or impaired renal function, and less than 140/90 mm Hg in the patients with prior cardiovascular disease.

Which of the following combinations of blood pressure medications was the best in reducing cardiovascular events and slowing the progression of nephropathy in patients with hypertension who were at high risk for such events?

		A. ACEI + Diuretics
		B. ACEI + CCB
		C. ACEI + Beta-blocker
		D. CCB + Beta-blocker

Explanation:

The correct answer is B

ACEI + CCB

Explanation:

• The Avoiding Cardiovascular Events through Combination Therapy in Patients Living with Systolic Hypertension - (ACCOMPLISH) trial showed that initial antihypertensive therapy with benazepril plus amlodipine was superior to benazepril plus hydrochlorothiazide in reducing cardiovascular morbidity and mortality.

• ACCOMPLISH ACCOMPLISH was a double-blind, randomized trial undertaken in five countries (USA, Sweden, Norway, Denmark, and Finland). 11 506 patients with hypertension who were at high risk for cardiovascular events were randomly assigned via a central, telephone-based interactive voice response system in a 1:1 ratio to receive benazepril (20 mg) plus amlodipine (5 mg; n=5744) or benazepril (20 mg) plus hydrochlorothiazide (12.5 mg; n=5762), orally once daily. Drug doses were force-titrated for patients to attain recommended blood pressure goals.

• The primary end point was the composite of death from cardiovascular causes, nonfatal myocardial infarction, nonfatal stroke, hospitalization for angina, resuscitation after sudden cardiac arrest, and coronary revascularization.

• The benazepril-amlodipine combination was superior to the benazepril-hydrochlorothiazide combination in reducing cardiovascular events in patients with hypertension who were at high risk for such events.

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TUTOR - CKD / ESRD / MBD

Test Id: 1869464d645156f064
QId: 167340

12 of 16

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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

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.

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TUTOR - Fluids and Electrolytes

Test Id: 1869464d645156f064
QId: 167254

13 of 16

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A 20 year-old-male was at a party where after dancing he ate a lot of cake because it was “delicious”. After 2-3 hours he developed sudden onset of weakness in all 4 limbs. He has had two similar episodes in the past. He was rushed to the nearest ER. On examination: P: 88/min, BP: 140/96 mm Hg, Pallor+, No thyroid enlargement. He is alert and oriented. There is no cranial nerve involvement and no neck muscle weakness. Motor power is grade 2-3 in all extremities, reflexes sluggish to absent. Sensory exam is normal. Laboratory results reveal the following:

pH 7.4

pCO2 40 mm Hg

paO2 98 mm Hg

HCO3 24 mEq/L

O2 saturation 98%

Na 140 mEq/L

K 2.2 mEq/L

Cl 103 mEq/

BUN 10 mg/dl

S.Cr 0.8 mg%

S. Ca 10.2 mg/dl

PO4 2.5 mg/dl

Mg 2.2 mg/dl

Urine Electrolytes

Urine Na 100 mEq/L

Urine K 15 mEq/L

Which of the following is the MOST likely diagnosis?

		A. Familial periodic paralysis.
		B. Renal tubular acidosis
		C. Primary hyperaldosternism.
		D. Thyrotoxic periodic paralysis

Explanation:

The correct answer is A

Familial periodic paralysis

Explanation:

In familial hypokalemic periodic paralysis, the hypokalemia is classically precipitated by carbohydrate load without any acid base disturbance. This typically occurs in the first or second decade of life. The low urinary K favors diagnosis of extra renal loss.

Renal tubular acidosis (Choice B) will have hypokalemia with metabolic acidosis and high urinary potassium, quadriparesis is uncommon in hypokalemia of RTA.

Primary hyperaldosteronism (Choice C) rarely presents with quadriparesis. Hypokalemia is associated with hypertension and metabolic alkalosis. High aldosterone and low renin levels are present.

Thyrotoxic periodic paralysis (Choice D) occurs after 20 years of age. Symptoms of thyrotoxicosis like palpitations, tachycardia, thyroid neck mass, low TSH with high T3 or high T4 is commonly seen. It is very common in Asians.

Educational Objective:

Differentiate between familial periodic paralysis and thyrotoxic periodic paralysis.

FAMILIAL PERIODIC PARALYSIS –

Hypokalemia in the absence of acidosis

Weakness is precipitated by carbohydrate load and Exercise

Low urinary potassium

THYROTOXIC PERIODIC PARALYSIS –

YOUNG, usually female, very common in ASIANS

Symptoms of thyrotoxicosis and Often NECK MASS.

LOW TSH and high T3 or T4.

IF YOU KNOW ABOVE POINTS NO MATTER HOW THE ABIM QUESTION IS FRAMED, YOU WILL BE ABLE TO ANSWER IT.

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TUTOR - Physiology

Test Id: 1869464d645156f064
QId: 165262

14 of 16

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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.

His laboratory investigation is reported as follows.

Characteristic	Value
Hemoglobin	14.2 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	4.4 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	101 mEq/L
Total Bilirubin	1.0 mg /dL
AST	16 U/L
ALT	18 U/L
Sr Albumin	4.0 g/dL
HBA1C	7.9%
Sr Calcium	10 mg/dL
Urine dipstick	pH- 5.4 Albumin-nil no blood no WBCs
24-hour urinary protein	76 milligrams/day

What is the MOST LIKELY incorrect statement regarding hyperfiltration stage of Diabetic Kidney Disease in this patient?

		A. Renal hyperfiltration is usually diagnosed when the GFR is more than 120 ml/min,which corresponds to a renal function that exceeds two standard deviation above mean GFR.
		B. Renal hyper filtration usually precedes microalbuminuria in type 1 diabetes mellitus.
		C. Renal hyper filtration is considered as a risk factor for future progression to chronic kidney disease (CKD) and end stage renal disease (ESRD) in type 1 DM.
		D. eGFR equations like MDRD equation can be used predict hyper filtration.

Explanation:

The Correct Answer is Option D : eGFR equations like MDRD equation can be used predict hyper filtration.

Explanation:

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.

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TUTOR - Acid - Base

Test Id: 1869464d645156f064
QId: 167322

15 of 16

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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

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.

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TUTOR - Hypertension

Test Id: 1869464d645156f064
QId: 16524

16 of 16

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Which of the following antihypertensive medications resulted in better blood pressure control and cardiovascular outcomes when combined with an ACE inhibitor?

		A. Beta blocker
		B. Calcium channel blocker
		C. Angiotensin Receptor Blocker
		D. Diuretics

Explanation:

The correct answer is B

Calcium channel blocker

Explanation:

The ACCOMPLISH trial has clearly shown that that an ACE inhibitor combined with a Calcium channel blocker (amlodipine) is better than an ACE inhibitor combined with a diuretic (hydrochlorothiazide). This study did not involve beta blockers or angiotensin receptor blockers.

The ACCOMPLISH trial was the first major clinical trial addressing the issue of combination therapy in 11,000 patients who were at high cardiovascular risk (with prior CAD, diabetes, and/or CKD). The patients were randomly assigned to combination therapy with benazepril (20 mg/day) combined with either amlodipine (5 mg/day) or Hydrochlorothiazide (12.5 mg/day).

The mean blood pressure was significantly lower in the Benazepril + Amlodipine group, with the primary end point also significant in this group. There was a similar benefit with the treatment combination of benazepril-amlodipine in the secondary end point of cardiovascular death compared to the group treated with a combination of amlodipine and hydrochlorothiazide.

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