Renal/Electrolytes Flashcards by ryan Devenyi

Paraneoplastic syndromes associated with renal cell carcinoma (4)

Polycythemia (ectopic EPO)
Hypercalcemia (bone mets, PTH-RP, and/or prostoglandins)
Elevated platelets
Secondary amyloidosis

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Mechanism of bleeding risk in uremia?

Treatment?

Platelet dysfunction (PT, PTT, and platelet count all normal, but platelet function impaired so bleeding time prolonged)

Treatment: desmopressin (increases release of factor VIII-vWF multimers that activate platelets) and/or HD

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Common side effect of IV EPO in ESRD

Rare but serious side effect

Common: Worsening hypertension

Rare but serious: Red cell aplasia

(Other common: headache, flu-like syndrome that responds to NSAIDs)

(Less common with subq EPO)

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Two complications of nephrotic syndrome

Atherosclerosis (hyperlipidemia from elevated liver synthesis of protein and lipids)
Thrombosis (loss of antithrombin III) (Especially in nephrotic syndrome due to membranous glomerulopathy)

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Cause of nephrotic syndrome associated with Hepatitis B

Membranous glomerulopathy

(Hep B also associated with membranoproliferative glomerulonephritis (MPGN) and polyarteritis nodosum (PAN), but these do not usually cause nephrotic syndrome)

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Cause of nephrotic syndrome associated with Hodgkin lymphoma

MInimal change disease (also associated with NSAIDs)

Most common cause in kids, but less so in adults

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Cause of nephrotic syndrome associated with HIV

Focal segmental glomerulosclerosis (also associated with AA-race and obesity)

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Specific pathologic finding in diabetic nephropathy

Nodular sclerosis, with Kimmelstiel-Wilson nodules

DIffuse glomerulosclerosis is more common in diabetic nephropathy, but is non-specific

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Mechanism of injury in membranous glomerulopathy

Immune complex deposition (so is membranoproliferative glomerulonephritis)

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Mechanism of injury in membranoproliferative glomerulonephritis

Immune complex deposition (so is membranous glomerulopathy)

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Glomerulonephritis associated with Hepatitis C

Memrbanoproliferative glomerulonephritis (MPGN)

Also less commonly associated with Hepatitis B

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Renal disease with sterile pyuria and WBC casts

Tubuloinsterstitial nephritis

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Disease with hemoptysis and nephritis/AKI

Goodpasture’s disease (anti-GBM)

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Linear IgG deposition in the glomerulus

Goodpasture’s disease (anti-GBM)

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What is a dangerous extrarenal complication of ADPKD?

Intracranial berry aneurysm (however, routine screening is not recommended in ADPKD patients)

(Can also have hepatic cysts, valvular heart disease, colonic diverticula, and hernias)

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Hypertension with microhematuria and a palpable flank mass

Autosomal dominant polycystic kidney disease (ADPKD)

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Cause of sudden generalized edema and hypertension

Acute nephritic syndrome (due to sudden decrease in GFR)

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Two causes of glomerulonephritis after URI? Time course of each? Association with complement?

IgA nephropathy: within 5 days, normal complement (mesangial IgA deposits)

Post-infectious GN: delayed (10-21 days), low C3 (also elevated ASO / DNAse B antibodies)

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Serologic association with post-infectious glomerulonpehritis

Anti-streptolyisin O (ASO) and anti-DNAse B antibodies

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Muddy brown casts

Acute tubular necrosis

WBC casts

Interstitial nephritis and pyelonephritis

RBC cases

Glomerulonephritis

Fatty casts

Nephrotic syndrome

Broad, waxy casts

Chronic renal failure

Hyaline casts

Nonspecific and not necessarily pathologic (can be seen in prerenal AKI but also just in concentrated urine)

Electrolyte abnormality from vomiting

Hypochloremic, hypokalemia, metabolic alkalosis

Electrolyte abnormality from diarrhea

Hyperchloremic metabolic acidosis

Lab test to distinguish between saline responsive and saline resistant metabolic alkalosis

Urine chloride Low (<20 mEq/L) in saline-responsive contraction alkalosis High in saline-resistant metabolic alkalosis (e.g. due to hyperaldosteronism - these patients have volume overload and are excreting NaCl)

One possible treatment for saline resistant metabolic alkalosis

Acetazolamide (blocks resorption of bicarb) | But causes hypokalemia, so use caution

Causes of saline-resistant metabolic alkalosis

1. Primary hyperaldosteronism 2. Cushing syndrome 3. Severe hypokalemia (<2 mEq/L)

Normal anion gap?

Normal AG: 6-12 mEq/L

Winter's formula?

Expected PaCO2 = 1.5*bicarb + 8, +/- 2

Causes of normal anion gap metabolic acidosis (2)

1. Diarrhea (vast majority of cases) | 2. Renal tubular acidosis

Renal tubular acidosis associated with autoimmune disease? | Most common autoimmune disease in the association?

Type 1 RTA Most commonly Sjogren's syndrome (also seen in RA)

Hyponatremia with high urine osmolarity and high urine sodium (>40)

SIADH | Retain free water due to inappropriate ADH, but excrete Na+ due to increased blood volume

Cancer classically associated with SIADH

Small cell lung cancer

Progression of EKG changes with hyperkalemia

1. Peaked T waves, short QT 2. Long PR, wide QRS 3. Loss of P wave 4. Conduction blocks, ectopic pacing, sine-wave patterns

Electrolytes in hypomagnesemia

1. Refractory hypokalemia (inhibits K+ resorption in kidney) | 2. Hypocalcemia (reduces PTH)

Electrolyte abnormalities in tumor lysis syndrome

1. Hyperuricemia (from metabolized nucleic acids) 2. Hyperkalemia 3. Hyperphosphatemia 4. Hypocalcemia (precipitates with phosphate)

Pretreatment that can help prevent AKI in tumor lysis syndrome

IV fluids and allopurinol or rasburicase (to prevent hyperuricemia) (Allopurinol: blocks xanthine oxidase and therefore uric acid production) (Rasburicase: recombinant uric oxidase, breaks down uric acid)

Infiltration that leads to hypoparathyroidism

Cancer, Wilson's, hemochromatosis

Effect of thiazides on calcium? Loop diuretics?

Thiazides: increase calcium reabsorption and therefore can lead to hypercalcemia. Loop diuretics: increase calcium excretion and therefore can lead to hypocalcemia

How do thiazides affect diabetes?

Worsen glucose intolerance by impairing insulin release and worsening glucose utilization

AE of furosemide not linked to kidney effects

Ototoxicity (hearing loss, tinnitus)

Three common types of nephrotoxic drugs that should be discontinued in AKI

NSAIDs, ACEIs, and aminoglycosides

Most common drug-induced chronic renal failure? Pathologic effects?

Analgesic nephropathy (usually combined analgesics, e.g. aspirin + naproxen) Leads to papillary necrosis and chronic tubulointerstitial nephritis

What presents with rash, arthralgias, hematuria, and WBC casts?

Interstitial nephritis | Make sure you don't confuse with reactive arthritis, but the "can't pee" there is urethritis/cervicitis, not renal

Who is at risk for contrast-induced nephropathy? What can be done to reduce this risk?

At-risk: Diabetics and baseline kidney disease Prevention: hydration and acetylcysteine