Nephrology

Question 1

Isopropyl alcohol ingestion

Answer 1

Patients with isopropyl alcohol ingestion have altered mental status, elevated osmolar gap, normal anion gap, and ketonuria/ketonemia. Treatment is mainly supportive.

Question 2

PTH dependant HyperCa

Answer 2

If urinary Ca >250mg / 24Hrs
⏩⏩ primary or tertiary hyperparathyroidism

If urinary Ca <100mg / 24Hrs
⏩⏩ Familial hypercalcemic hypocalciuria

Question 3

Causes of hypercalcemia in patients with low PTH (independent)
Normal PTHrP, 25 & 1,25 Vit D

Answer 3

Hyperthyroidism
Multiple myeloma
Adrenal tumor
Acromegaly
Vitamin A toxicity
Immobilization
Milk-alkali syndrome

Question 4

Acute interstitial nephritis
Causes

Answer 4

Medications (eg, antibiotics, NSAIDS, PPIs)*
Rheumatologic disease (eg, SLE, Sjögren syndrome,sarcoidosis)
Infections (eg, Legionella, tuberculosis, CMV)

Question 5

Acute interstitial nephritis
Clincal presentation

Answer 5

New medication exposure, Acute kidney injury, Arthralgias, malaise
Classic triad of fever, skin rash & eosinophilia rarely
Urinalysis: WBCs & WBC casts + mild RBCs & proteinuria
Peripheral eosinophilia + urine eosinophils
Renal biopsy: tubulointerstitial inflammation & edema

Question 6

Acute interstitial nephritis treatment

Answer 6

Offending medications should be discontinued immediately. Renal biopsy is diagnostic but is not required in patients whose renal function improves after medication withdrawal
Glucocorticoids are often used in patients who fail to improve after medication withdrawal, although the benefits remain unclear

Question 7

Extrarenal complications of Adult polycystic kidney disease

Answer 7

• Intracranial aneurysms
• Hepatic and pancreatic cysts
• Cardiac valve disease and aortic root dilatation
• Diverticulosis

Question 8

ADPKD, intracranial aneurysm screening

Answer 8

Guidelines recommend screening patients with previous aneurysm rupture, family history of intracerebral bleed or aneurysm, and high-risk occupations (eg, pilots).

screening is best performed with time-of-flight magnetic resonance angiography, which does not require gadolinium contrast and can be done at any glomerular filtration rate level.
Computed tomography angiography is an alternate screening method.

Question 9

Causes of NAGMA

Answer 9

• Diarrhea
• Fistulae (eg, pancreatic, ileocutaneous, etc.)
• Carbonic anhydrase inhibitors
• Renal tubular acidosis
• Ureteral diversion (eg, ileal loop)
• Iatrogenic

Check Urine Anion gap
Positive ⏩ Renal cause
Negative ⏩ Gi cause

Question 10

Toluene ingestion

Answer 10

Toluene is inhaled and then converted by the liver to hippuric acid, which can cause an elevated anion gap metabolic acidosis in the early stages.

However, hippuric acid is rapidly excreted by the kidneys along with sodium and potassium. There is also limited renal ammonium production and eventual distal RTA.
The resultant serum hypokalemia leads to diffuse weakness, low level of rhabdomyolysis, and hypophosphatemia. Treatment is largely supportive with fluid and electrolyte repletion

Question 11

Salicylate toxicity
Presentation

Answer 11

encephalopathy

anion gap metabolic acidosis (AGMA) and an additional respiratory alkalosis.

auditory (eg, tinnitus with hearing loss), gastrointestinal (eg, gastritis, vomiting), and pulmonary (eg, noncardiogenic edema)

Question 12

Salicylate toxicity
Management

Answer 12

1- involves serum and urinary alkalinization via intravenous bicarbonate administration even in the setting of alkalosis (as long as pH <7.60). Serum alkalinization promotes salicylate movement out of cells while urinary alkalinization increases the rate of renal excretion.

Acetazolamide should not be given; although it alkalinizes the urine, this occurs at the expense of serum acidification with a resultant salicylate movement into cells.

2-Hemodialysis should be considered in severe cases (eg, pulmonary or cerebral edema, renal failure).

Intubation should be avoided because adequate hyperventilation is difficult to maintain mechanically in these patients, and they are highly susceptible to worsening acidemia with a drop in minute ventilation

Question 13

Creatinine and Bactrim

Answer 13

By decreasing creatinine secretion, both trimethoprim and cimetidine can result in an increased serum creatinine without decreasing the glomerular filtration rate.

Question 14

Bk polyoma virus
Introduction

Answer 14

In renal transplant recipients, the BK form of polyoma virus produces tubulointerstitial nephritis and, less commonly, ureteric stenosis.

The mean time of onset of BK infection is 10-15 months after transplantation.
BK viral infection is most common in older men with type 2 diabetes mellitus and rejection episodes with significant immunosuppression.

There are no characteristic clinical manifestations other than loss of renal function.

Question 15

Bk polyoma infection
Diagnosis and treatment

Answer 15

The presence of cells with a single large basophilic intranuclear inclusion found on urine cytology suggests but does not prove BK infection.

Serology is not as useful as many in the general population have antibodies against the virus.
Renal biopsy findings can be similar to those in other viral infections (eg, cytomegalovirus). As a result, diagnosis requires renal biopsy showing characteristic cytopathology plus positive antibodies directed specifically against BK on immunohistochemistry tests.

Biopsy sometimes misses the diagnosis, and at least 2 biopsy cores may be required in suspected patients.

The primary treatment is reduction of immunosuppression.

Question 16

Calcineurin inhibitor nephrotoxicity

Answer 16

Patients can have declining glomerular filtration rates and a variety of metabolic abnormalities, including hyperkalemia, hyperuricemia, hypophosphatemia, hypomagnesemia, hypercalciuria, and possibly metabolic acidosis.

Significant hypertension may also be present. Toxicity is dose-dependent. Calcineurin inhibitors are metabolized by cytochrome P450 3A4; levels are increased by other drugs that are metabolized by this enzyme (eg, azole antifungals, macrolides, non-dihydropyridine calcium channel blockers).

Biopsy is often required to rule out acute rejection.
Acute calcineurin inhibitor toxicity is usually reversible with drug cessation, although some patients develop residual chronic renal dysfunction.

Question 17

Nephrogenic DI

Answer 17

Lithium can be associated with nephrogenic DI in up to 20-40% of patients. Symptomatic patients should discontinue lithium. Patients who cannot stop lithium may be treated with salt restriction and a trial of diuretics (i.e., amiloride or thiazides) with careful monitoring of renal function and serum lithium levels.

Question 18

CKD-MBD
Osteitis fibrosa cystica

Answer 18

Lab findings
• PTH >450 pg/mL
• High ALP

Treatment
Decrease PTH
• Dietary phosphate restriction, phosphate binders
• Vitamin D analogues
• Calcimimetics* i.e. cinacalcet in dialysis patients only

Question 19

CKD-MBD
Adynamic bone disease

Answer 19

Lab findings
• PTH <100 pg/mL
• Low or normal ALP

Treatment
Increase PTH:
• Discontinue vitamin D analogues
• Switch to non-calcium- containing phosphate binders
• Use low-calcium dialysate in dialysis patients only

Question 20

Contrast induced nephropathy prevention

Answer 20

Preventive measures include using the smallest possible volume of contrast media, holding nonsteroidal anti-inflammatory drugs, and optimizing volume status to maximize renal perfusion (ie, IV normal saline in most patients, diuretics if volume overload is present).

No role of holding ACE Is or ARBs prior contrast administration

Question 21

Scleroderma renal crisis

Answer 21

Risk factors:
• Diffuse, aggressive skin involvement, tendon friction rubs
• High-dose glucocorticoid therapy
• Anti-RNA polymerase III antibodies (lower risk with anticentromere antibodies)

Presentation:
• Acute kidney injury
• Moderate or severe hypertension/malignant hypertension
• Proteinuria, normal urine sediment
• Microangiopathic hemolytic anemia

Treatment:
Oral ACE Inhibitors captopril, back to baseline within 72Hrs

Question 22

Post obstruction diuresis

Answer 22

Chronic partial bilateral urinary obstruction can result in normal or slightly increased urine volume, while complete bilateral obstruction causes anuria. Relief of the obstruction leads to post-obstructive diuresis (500-1000 cc/hr) that can be worsened by trying to match volume repletion with urine output.

There are no controlled studies to guide management; however, most experienced clinicians replace the patient’s body volume with either isotonic or half normal saline at a rate <50% of urine volume (eg, ~200 cc/hr in this patient with urine output ~600 cc/hr) and adjust the rate based on the patient’s response and subsequent volume status

Question 23

Hyperphosphatemia &FGF 23

Answer 23

FGF-23, the major phosphaturic hormone. FGF-23 decreases the expression of the sodium phosphorous cotransporter in the proximal tubule. In tumoral calcinosis, FGF-23 activity is decreased; therefore, there is increased phosphorous absorption in the proximal tubule resulting in hyperphosphatemia and metastatic calcifications

Question 24

Mild microscopic hematuria

Answer 24

The presence of isolated dysmorphic hematuria in a young patient typically indicates very mild glomerular disease (most often IgA nephropathy) or thin glomerular basement membrane disease related to a type IV collagen defect. Thin glomerular basement membrane disease is more likely if there is a strong family history of hematuria, which is found in 30% to 50% of cases, and no family history of chronic kidney disease.

Question 25

Infection related glomerulonephritis

Answer 25

The biopsy shows a proliferative glomerulonephritis on light microscopy with immunofluorescence of C3 and IgA and subepithelial hump-like deposits on electron microscopy.

Question 26

Acid-Base disorder in cirrhotic patients

Answer 26

Chronic respiratory alkalosis is the most common acid-base abnormality in cirrhosis and is in part a sequela of progesterone accumulation caused by impaired hepatic metabolism. Progesterone accumulation leads to central stimulation of ventilation, which increases the respiratory rate and tidal volume (ie, hyperventilation).

Question 27

Medications Causing NAGMA

Answer 27

-CA inhibitors (Acetazolamide & Topiramate)
-Chemotherapy (Ifosfamide & Cisplatin)
-Antibiotics (Bactrim & Aminoglycosides)
-Lithium
-Ampho B
-Inhaled Toluene
-Rifampin
-Pentamidine

Question 28

Renal Athero-embolic disease

Answer 28

Risk factors:
Aortic Arteriography, angioplasty or surgery

Clinical presentation:
-AKI after 1-2 weeks from procedure
-Urine sediments (Hematuria, Eosinophiluria, WBC, and mild proteinuria )
-Peripheral eosinophilia and Hypocomplementemia
-Digital cyanosis or gangrene in toes, intact pulses
-Livedo reticularis

Question 29

ACEIs ARBs in CKD

Answer 29

• In patients with chronic kidney disease, kidney func- tion and serum potassium levels should be reassessed 2 to 3 weeks after initiation of an ACE inhibitor or angiotensin receptor blocker.

• Following initiation of an ACE inhibitor or angiotensin receptor blocker, a >30% increase in serum creatinine levels necessitates decreasing the dose of or discontin- uing these agents.

Question 30

ESRD and RCC

Answer 30

Patients with end-stage kidney disease are at increased risk for renal cell carcinoma
Screening for renal cell carcinoma in patients with end-stage kidney disease and acquired cystic kidney disease may be reasonable in patients with a longer life expectancy.

Question 31

Indication for kidney biopsy

Answer 31

• Glomerular hematuria
• significant increase in proteinuria
• Acute or chronic kidney injury without clear cause
• kidney transplant dysfunction or monitoring

Question 32

Management of GERD in CKD patients

Answer 32

• Proton pump inhibitors may contribute to the devel- opment and progression of chronic kidney disease and should be avoided.

• H₂ blocker therapy can be considered for patients with advanced chronic kidney disease provided appropriate dosing is used.

Question 33

Management of chronic hypertension during pregnancy

Answer 33

• For pregnant women with chronic hypertension, guidelines recommend only treating persistent sys- tolic ≥160 mm Hg or diastolic ≥110 mm Hg blood pressure in the absence of end-organ damage to avoid overtreatment of hypertension and associated fetal risk.

• Treatment of chronic hypertension (<160/110 mm Hg) during pregnancy is not associated with improved fetal outcomes.

Blood pressure goals with medications are 120-159/80-109 mm Hg. First-line agents are labetalol, nifedipine, and methyldopa.

Question 34

Renal tubular acidosis

Answer 34

Type 2 (proximal) renal tubular acidosis is character- ized by a normal anion gap metabolic acidosis, hypokalemia, glycosuria (without hyperglycemia), low-molecular-weight proteinuria, and renal phos- phate wasting.

Type 1 (hypokalemic distal) renal tubular acidosis is characterized by a normal anion gap metabolic acidosis, hypokalemia, urine pH >6.0, and calcium phosphate kidney stones.

Question 35

Nephrotic syn in African descent

Answer 35

• Focal segmental glomerulosclerosis is the most common form of the nephrotic syndrome in Black patients, likely mediated in large part by variants in the APOL1 gene

Question 36

Management of Stage 1 Hypertension

(systolic blood pressure [SBP] of 130-139 mm Hg or diastolic blood pressure [DBP] of 80-89 mm Hg)

Answer 36

• Adults with stage 1 hypertension who have an esti- mated 10-year atherosclerotic cardiovascular disease event risk of <10% should be managed initially with nonpharmacologic therapy.

• Adults with stage 1 hypertension who have an estimated 10-year atherosclerotic cardiovascular disease event risk of ≥10% should be managed initially with nonpharmacologic and antihypertensive drug therapy.

Question 37

Kidney stones in pregnancy
Diagnosis

Answer 37

Ultrasonography is readily available, inexpensive, and very safe and is a useful first study in evaluating neph- rolithiasis.

• Kidney ultrasonography is the preferred diagnostic test for suspected nephrolithiasis in pregnant women.

Question 38

Membranoproliferative glomerulonephritis

Answer 38

• The immune complex form of membranoproliferative glomerulonephritis is associated with infectious, autoimmune, or malignancy-associated etiologies.

• The most common etiology of immune complex membranoproliferative glomerulonephritis is infectious, specifically hepatitis C virus infection.

Question 39

Management of volume overload in nephrotic syndrome

Answer 39

In patients with the nephrotic syndrome and refractory edema despite high-dose loop diuretics, adding a thiazide diuretic and/or a potassium-sparing diuretic is the appropriate next step in management

Question 40

Cellcept and pregnancy

Answer 40

• Mycophenolate mofetil is teratogenic and is contrain- dicated in pregnancy.
• Documented risks with mycophenolate mofetil use include first-trimester pregnancy loss and fetal malformations of the distal limbs, heart esophagus, kidneys, and cleft lip and palate.

Mycophenolate mofetil is also contraindicated in women who are breastfeeding because the drug is excreted into breast milk.

If continued immuno suppression is required, be switched to azathioprine, which is generally safer and well tolerated in pregnancy

• In diseases in which mycophenolate mofetil is used, patients should show stable disease for 3 to 6 months following discontinuation of the agent before proceeding with pregnancy.