Nephrology

Question 1

Goodpasture disease

Answer 1

Autoimmune type 2 sensitivity reaction.
Lung symptoms usually precede kidney symptoms and include hemoptysis, cough, shortness of breath, and chest pain.
Kidney symptoms usually include blood and protein in the urine, unexplained edema, elevated blood pressures.
kidney biopsy: crescentic glomerulonephritis pathology with linear anti-GBM antibodies.

Question 2

The 2 most important cause of metabolic acidosis with normal anion gap?

Answer 2

Renal tubular acidosis and diarrhea.

Question 3

Renal tubular acidosis type I

Answer 3

The distal tubule cannot generate bicarbonate, the acid cannot be excreted into the tubule = raising the PH in the urine.

Question 4

Renal tubular acidosis Type II

Answer 4

proximal tubule cannot reabsorb bicarbonate.

Question 5

Renal tubular acidosis type IV

Answer 5

Occurs most often in diabetes
Decrease amount of effect of aldosterone=loss of sodium and retention of potassium and hydrogen ions.
Urine PH low

Question 6

Patient shows signs of nephrotic syndrome and has Hodgkin’s lymphoma (HL), the nephropathy the patient is most likely experiencing?

Answer 6

The most common nephropathy associated with Hodgkin lymphoma and other hematologic malignancies minimal change disease.

Question 7

The most common nephropathy associated with solid tumors is?

Answer 7

Membranous nephropathy (immune complex mediated).

Question 8

Membranoproliferative glomerulonephritis

Answer 8

Nephrotic syndrome
Type I is generally a slower disease secondary to systemic lupus erythematosus (SLE), chronic hepatitis C, or hepatitis B. Type II is a more aggressive disease caused by autoimmune activation of complement by nephritic factor, an autoantibody against C3.

Both: low serum C3; however only type II is associated with C3 nephritic factor.

Biopsy: Type I, and type II shows intramembranous dense deposits.

Question 9

Minimal change disease in adults

Answer 9

in association with Hodgkin’s and non-Hodgkin’s lymphomas and leukemia.

Question 10

Most common cause of nephrotic syndrome in adults?

Answer 10

Focal segmental glomerulosclerosis

Question 11

Hyposthenuria in sickle cell disease patients.

Answer 11

the defect in urinary concentration is related to sickled erythrocytes that restrict blood flow in the renal medulla, impairing the kidney’s ability to create a gradient needed to concentrate the urine.
Both antidiuretic hormone generation and urinary diluting capacity remain unperturbed.
Neither water deprivation nor desmopressin will result in a significant increase in urine osmolality.

Question 12

The treatment of an acute exacerbation of Goodpasture syndrome?

Answer 12

Methylprednisolone, plasmapheresis, and cyclophosphamide.

Question 13

Which other abnormality is autosomal dominant polycystic kidney disease associated with?

Answer 13

Polycystic liver disease, berry aneurysms and mitral valve prolapse (a mid-systolic click).

Question 14

Metabolic alkalosis

Answer 14

Generated by four factors: volume depletion, chloride depletion, hypokalemia, and aldosterone excess.
These factors either increase the rate of bicarbonate reabsorption or decrease the rate of bicarbonate secretion.

Main clinical settings to consider:

1. Loss of gastric fluid - nasogastric drainage or vomiting
2. Diuretic therapy
3. Mechanical ventilation of patients with chronic respiratory acidosis
4. Primary hyperaldosteronism

Question 15

Cooling dialysate benefits

Answer 15

Can improve hemodynamic stability, reduce hypotension, and improve cardiac function during hemodialysis. It may also reduce the risk of cardiovascular mortality and brain injury.

Question 16

Acute kidney injury summary

Answer 16

Pre renal AKI oliguria, urine sodium <20meq/L, bun:cREAT >20:1, increase urine osmolarity, a low FENa (<1%).

Intrarenal AKI urine sodium <20meq/L, bun:CREAT <15:1, low urine osmolarity, FENa (>1%).
are unable to concetrate urine, a sign of a nephron damage.

Post renal AKI bun:cREAT <20:1, FENa (>1%), variable urine osmolarity, variable urine Na, depending on if it is early or late.

Question 17

A diabetic patient with a non-anion gap metabolic acidosis, hyperkalemia, and renal insufficiency should be suspected of having?

Answer 17

Type 4 renal tubular acidosis
The lack of effect of aldosterone leads to decreased secretion of acid as ammonium (NH4+) and potassium retention.
Type 4 RTA may occur in the setting of diabetic nephropathy and can be exacerbated by drugs that inhibit the renin-angiotensin-aldosterone system, such as ACE inhibitors or ARBs.

Question 18

Membranoproliferative glomerulonephritis

Answer 18

Nephrotic syndrome with two distinct forms.

Type I: Slower disease secondary to systemic lupus erythematosus, chronic hepatitis C, or hepatitis B.

Type II is a more aggressive disease caused by autoimmune activation of complement by nephritic factor, an autoantibody against C3.

Both share the laboratory findings of low serum C3.
Biopsy: Type I shown “tram-tracking” , and type II shows intramembranous dense deposits.

Treatment: prednisone with or without plasmapheresis or interferion-alpha, and prognosis is poor.

Question 19

Renal osteodystrophy would present with?

Answer 19

Low calcium, high phosphate, and low energy fractures.

Question 20

Ethylene glycol and acute kidney injury

Answer 20

Ethylene glycol is converted to glycolate, which is toxic to renal tubules and can lead to acute kidney injury.
Glycolate is then metabolized to oxalate, causing tubular obstruction and oliguric renal failure by forming calcium oxalate crystals.

Question 21

Hyperlipidemia in nephrotic syndrome

Answer 21

Is common and linked to increased liver lipoprotein production due to low oncotic pressure.

Question 22

Nephrotic syndrome complications

Answer 22

• Accelerated atherosclerosis: decreased plasma oncotic pressure stimulates increased hepatic protein synthesis, including lipoprotein synthesis and reduced LDL clearance due to PCSK9.
  -Thrombotic events from loss of natural anticoagulants.
• Bacterial infections from loss of immunoglobulins.
  -Vitamin D deficiency from loss of its binding protein.
  -Anemia from loss of transferrin and erythropoietin.

Question 23

Chronic kidney disease and hyperkalemia

Answer 23

Patients with chronic kidney disease on renin-angiotensin inhibitors may develop mild to moderate hyperkalemia, managed with a low-potassium diet and oral cation exchange agents like patiromer or zirconium cyclosilicate, which bind potassium in the colon for fecal excretion.

Question 24

First-line treatments for renal artery stenosis (RAS)

Answer 24

ACE inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) due to their ability to lower angiotensin II levels, improving blood pressure and dilating glomerular efferent arterioles.
They provide long-term nephroprotection by reducing intraglomerular pressures and lower the risk of myocardial infarction, stroke, and end-stage renal disease.

Question 25

Minimal change disease pathogenesis

Answer 25

Dysregulation of T cell subpopulations that release cytokines that damage the capillary of the glomerulus, leading to epithelial podocyte injury.

Question 26

A voiding cystourethrogram is recommended to?

Answer 26

Evaluate urologic abnormalities in children with ≥2 febrile UTIs, abnormal renal ultrasound, high fever with unusual pathogens, or signs of chronic kidney disease

Question 27

Metabolic acidosis compensation

Answer 27

First the kidneys compensate by increasing HCO3− reabsorption and H+ excretion, leading to higher urinary chloride excretion, with most excreted H+ as ammonium (NH4+) or dihydrogen phosphate (H2PO4−). After several days the lungs compensate.

Question 28

Nitrofurantoin and trimethoprim-sulfamethoxazole in pregnancy

Answer 28

Used for acute cystitis in pregnancy, but nitrofurantoin is ineffective for pyelonephritis, and trimethoprim-sulfamethoxazole is avoided in the third trimester due to the risk of neonatal kernicterus.

Question 29

Severe obesity and nephrotic syndrome

Answer 29

Obesity is a risk factor for secondary focal segmental glomerulosclerosis from hyperfiltration injury due to increased blood volume.

Question 30

Urinalysis in rhabdomyolysis

Answer 30

Positive blood but no RBCs on urine microscopy, with pigmented casts.

Question 31

Analgesic nephropathy

Answer 31

1. Prolonged use of combination analgesics, leading to acetaminophen-induced glutathione depletion and direct renal toxicity from aspirin/NSAIDs. 2. Chronic interstitial nephritis and possibly papillary necrosis. 3. History of chronic pain, often asymptomatic but may include malaise, fatigue, and flank pain. 4. Urinalysis: WBCs, WBC casts, mild proteinuria, and hematuria if papillary necrosis is present. 5. Imaging: small kidneys with calcification and irregular contours.

Question 32

Renovascular hypertension

Answer 32

Such as renal artery stenosis, is a common cause of resistant hypertension. Clinical indicators: -serum creatinine increase >30% after ACE inhibitor or angiotensin receptor blocker initiation. - recurrent flash pulmonary edema. -diffuse atherosclerosis -asymmetric kidney size - abdominal bruit.

Question 33

Allergic Interstitial nephritis

Answer 33

Acute renal failure, fever, rash, and a recent history of antibiotic, diuretics and NSAIDs use, along with WBC casts in urinalysis. Symptoms can also include arthralgias and eosinophiluria. Typically appearing 5 days to several weeks post-exposure. It can also result from infections like Legionella, Mycobacterium tuberculosis, and Streptococcus.

Question 34

Enteric hyperoxaluria

Answer 34

In malabsorption syndromes, such as Crohn disease or after gastric bypass, excess fatty acids form complexes with calcium, reducing its availability to bind dietary oxalate>>>>>> increased oxalate absorption and hyperoxaluria = calcium oxalate stones.

Question 35

Alport syndrome

Answer 35

Inherited disease (X linked) affecting type IV collagen in the glomerular basement membrane, cochlea, and eye, typically presenting in boys under 10 with gross hematuria following a respiratory infection. Asymptomatic microscopic hematuria may precede gross hematuria, which can recur with hypertension, proteinuria, and chronic renal failure. Sensorineural hearing loss and anterior lenticonus.

Question 36

Muddy brown granular cast Red blood cell casts White blood cell casts Fatty casts Broad and waxy casts RELATED WITH?

Answer 36

1. Muddy brown granular cast - Acute tubular necrosis 2. Red blood cell casts - Glomerulonephritis 3. White blood cell casts - Interstitial nephritis and pyelonephritis 4. Fatty casts - Nephrotic syndrome 5. Broad and waxy casts - Chronic renal failure

Question 37

Classification of lupus nephritis

Answer 37

The histologic classification is related to the glomerular site (mesangial, subendothelial, subepithelial) of immune complex (IC) deposits formed by autoantibodies against nuclear self-antigens (eg, anti–double-stranded DNA bound to DNA). 1. Asymptomatic proteinuria and/or microscopic hematuria for mesangial ICs (classes I and II). 2. Glomerulonephritis for subendothelial ICs (classes III and IV). 2.1 Subepithelial ICs (class V) produce nephrotic syndrome. 3. Class VI lupus nephritis describes end-stage scarring of >90% of glomeruli that is unlikely to benefit from treatment. Treatment is determined by histologic class.

Question 38

The most common cause of death in patients with end-stage renal disease

Answer 38

Cardiovascular disease (coronary artery disease, stroke)

Question 39

End-stage renal disease and ulnar neuropathy.

Answer 39

Patients with end-stage renal disease can develop ulnar neuropathy due to positioning during hemodialysis sessions; chronic uremia causes further vulnerability due to generalized muscle wasting and loss of subcutaneous soft tissue.

Question 40

Fibrovascular displasia

Answer 40

Cause of renal artery stenosis in young patients. Due to activation of the renin angiotensin aldosterone system and high concentration of angiotensin II secondary hypertesion develops. is common to auscultate a bruit on the side of the renal artery stenosis.

Question 41

Nocturnal primary enuresis treatment

Answer 41

Desmopressin is the first-line pharmacotherapy for nocturnal enuresis. It can provide immediate improvement when behavioral modifications and alarm therapy have failed.