Renal/Electrolytes Flashcards
Sign of uremic encephalopathy on exam?
Treatment?
Sign: asterexis (flapping hand tremor)
Treatment: Emergent HD
Classic triad of renal cell carcinoma
- Flank pain
- Hematuria (invasion of colelcting system)
- Palpable abdominal mass
(Rarely seen, indicates late stage disease)
Paraneoplastic syndromes associated with renal cell carcinoma (4)
- Polycythemia (ectopic EPO)
- Hypercalcemia (bone mets, PTH-RP, and/or prostoglandins)
- Elevated platelets
- Secondary amyloidosis
Most common cause of death in dialysis patients
Cardiovascular disease (tend to have other risk factors, and ESRD is an independent risk factor)
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
When is EPO given in ESRD
If hemoglobin <10 after iron supplementation
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)
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)
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)
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
Cause of nephrotic syndrome associated with HIV
Focal segmental glomerulosclerosis (also associated with AA-race and obesity)
What is the earliest sign of diabetic nephropathy?
Glomerular hyperfiltration
Leads to damage via to intraglomerular hypertension, ACEIs protect against this
Medications protective against diabetic nephropathy
ACEIs (reduce intraglomerular hypertension)
Specific pathologic finding in diabetic nephropathy
Nodular sclerosis, with Kimmelstiel-Wilson nodules
DIffuse glomerulosclerosis is more common in diabetic nephropathy, but is non-specific
Early pathologic finding in hypertensive kidney disease? Later finding?
Early: benign nephrosclerosis (hypertropy and intimal medial fibrosis)
Late: glomerulosclerosis (loss of capillary surface area with glomerular and peritubular fibrosis)
Mechanism of injury in membranous glomerulopathy
Immune complex deposition
Mechanism of injury in mebranoproliferative glomerulonephritis
Immune complex deposition
Glomerulonephritis associated with Hepatitis C
Memrbanoproliferative glomerulonephritis (MPGN)
Also less commonly associated with Hepatitis B
Renal disease with sterile pyuria and WBC casts
Tubuloinsterstitial nephritis
Disease with hemoptysis and nephritis/AKI
Goodpasture’s disease (anti-GBM)
Linear IgG deposition in the glomerulus
Goodpasture’s disease (anti-GBM)
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)
Hypertension with microhematuria and a palpable flank mass
Autosomal dominant polycystic kidney disease (ADPKD)
Cause of sudden generalized edema and hypertension
Acute nephritic syndrome (due to sudden decrease in GFR)
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)
Serologic association with post-infectious glomerulonpehritis
Anti-streptolyisin O (ASO) and anti-DNAse B antibodies
First test in postoperative oliguria
Bladder scan (in cast of postoperative urinary retention, due to ineffective detrusor muscle)
(Straight cath is an alternative that is diagnostic and therapeutic)
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
Phases of metabolic alkalosis
Generation (excess bicarb production) and Maintenance (prevention of renal bicarb excretion)
What is a common reason for the maintenance of metabolic alkalosis?
Hypovolemia
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
- Primary hyperaldosteronism
- Cushing syndrome
- 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)
- Diarrhea (vast majority of cases)
2. Renal tubular acidosis
Electrolyte abnormality in severe diarrhea
Hypokalemia with normal anion gap metabolic acidosis
Types of renal tubular acidosis?
Urine pH in each
K+ level in each?
Type 1: Distal failure to excrete
Type 2: Proximal failure to resorb bicarb rare)
Type 4: Aldosterone resistance
Urine pH: Alkalotic with type 1 (unable to acidify) normally acidic in type 2 and 4
K+: Hypokalemia in type 1 and 2, hyperkalemia in type 4
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)
Complications of methanol poisoning? Ethylene glycole poisoning?
Methanol: vision changes
Ethylene glycol: hypocalcemia and AKI (metabolized to oxalate, precipitates with calcium including in kidney)
Metabolic acidosis with osmolar gap
Due to alcohols: ethanol, methanol, ethylene glycol
Acid-base in salicylate toxicity
- Respiratory alkalosis early (stimulation of respiratory centers)
- Anion gap metabolic acidosis later
Acid-base disorder with tinnitus
Salicylate poisoning
Fluid replacement in hypernatremia
Unstable: volume replacement with normal saline
Stable: slow replacement with D5 1/2NS
Most common causes of hypernatremia (2)
- Loss of hypotonic fluids
2. Decreased free water intake
Hyponatremia without low osmolarity (2)
- Hyperglycemia
2. Advanced renal failure
Hyponatremia with low urine osmolarity
Primary polydipsia
Hyponatremia with low urine sodium (<25)
Resulting from intravascular hypervolemia leading to ADH secretion
Hyponatremia with high urine sodium (>25)
SIADH, adrenal insufficiency, hypothyroidism
Hyponatremia with high urine osmolarity and high sodium (>40)
SIADH
Retain free water due to inappropriate ADH, but excrete Na+ due to increased blood volume
Treatment of mild SIADH
Treatment of severely symptomatic SIADH
Mild: Water restriction, +/- salt tablets
Severe: Hyperstonic saline
Interpretation of vasopressin suppression test in high urine output
Primary polydipsia: urine concentrated with free water restriction
Central DI: urine concentrates with vasopressin
Nephrogenic DI: urine remains dilute with vasopressin
Treatment of nephrogenic DI
- Check for hypercalcemia, and correct if found
- If due to lithium, discontinue (but may not reverse fully)
- Otherwise, hydrochlorothiazide
Cancer classically associated with SIADH
Small cell lung cancer
Electrolyte abnormalities in primary adrenal failure
Hyperkalemia, hyponatremia, non-anion gap metabolic acidosis
When does hyperkalemia require emergent treatment?
- Serum K+ >7
- Rapidly rising K+
- EKG changes
Rapid treatment of severe hyperkalemia
- Calcium gluconate
- IV insulin + glucose
- Beta agonists (e.g. inhaled albuterol)
- Sodium bicarbonate
Progression of EKG changes with hyperkalemia
- Peaked T waves, short QT
- Long PR, wide QRS
- Loss of P wave
- Conduction blocks, ectopic pacing, sine-wave patterns
Medications that can lead to hyperkalemia
- NSAIDs
- ACEIs/ARBs
- Beta blockers
- Digoxin
- K+-sparing diuretics
Electrolytes in hypomagnesemia
- Refractory hypokalemia (inhibits K+ resorption in kidney)
2. Hypocalcemia (reduces PTH)
Electrolyte abnormalities in tumor lysis syndrome
- Hyperuricemia (from metabolized nucleic acids)
- Hyperkalemia
- Hyperphosphatemia
- 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)
Total calcium correction with hypoalbuminemia
Corrected Ca = Measured Ca + 0.8*(4-albumin)
Relationship between acid-base and free calcium
H+ and Ca2+ essentially compete for binding to albumin, so acidosis increases free Ca2+, and alkalosis decreases free Ca2+
Infiltration that leads to hypoparathyroidism
Cancer, Wilson’s hemochromatosis
Causes of hypocalcemia
- Hypoparathyroidism
- Metabolic causes: vitamin D deficiency, CKD
- Precipitation: pancreatitis, hyperphosphatemia, osteoblastic metastasis
Symptoms of severe hypercalcemia
- Stones: kidney and gall stones
- Bones: bone pain
- Groans: abdominal pain, N/V, constipation
- Thrones: polyuria and dehydration
- Psychiatric overtones: depression, anxiety, cognitive dysfunction, insomnia, coma
Short-term treatment of severe hypercalcemia?
Long-term hypercalcemia treatment?
Short-term: Calcitonin + NS
Long-term: Bisphosphonates
Paraneoplastic syndrome associated with squamous cell cancer of the lung
Hypercalcemia due to PTHrp
SCa++mous
Treatment of milk alkali syndrome
Isotonic saline and furosemide (causes Ca2+ excretion)
Electrolyte abnormalities in milk alkali syndrome
- Hypercalcemia
- Metabolic alkalosis (alkali intake + renal dysfunction)
- Hypophosphatemia
- Hypomagnesemia
Causes of hypercalcemia with elevated/normal PTH
- Primary hyperparathyroidism
2. Familial hypocalciuric hypercalcemia (genetic mutation in calcium sensor that inhibits PTH release)
Complication of overly rapid correction of hyponatremia?
Overly rapid correction of hypernatremia?
Hyponatremia correction: Osmotic demyelination syndrome
Hypernatremia correction: cerebral edema
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 discontinues in AKI
NSAIDs, ACEIs, and aminoglycosides
Effect of NSAIDs on renal arterioles?
ACEIs?
NSAIDs: constrict the afferent arteriole (preventing prostoglandins from dilating it)
ACEIs: dilates efferent arterioles more than afferent (angiotensin constricts efferent more than afferent)
(Both reduce GFR and can worsen pre-renal azotemia)
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
Most common cause of interstitial nephritis
Drug-induced (70% of cases)
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
Common triggers of drug-induced interstitial nephritis (7)
- Penicillins
- Cephalosporins
- Sulfonamides (e.g. TMP-SMX)
- Rifampin
- NSAIDs
- Phenytoin
- Allopurinol
How can renal toxicity from acyclovir be prevented?
Aggressive hydration (toxicity is from acyclovir crystals forming in the urine)
What electrolyte disturbance can result from TMP-SMX?
Hyperkalemia:
(Trimethroprim can block ENaC and lead to hyperkalemia, as you lose sodium and water but not potassium, mimics the K-sparing diuretic amiloride)
What electrolyte disturbance can result from albuterol?
Hypokalemia (drives K+ into cells - goes for any beta agonist)
One contraindication for metformin
Renal failure (creatinine >1.5 in men, >1.4 in women) due to risk of lactic acidosis
(FDA relaxed this CI but it is still a relative CI)
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 acetylcystein
Common cause of drug-induced DI
Lithium
Most common glomerulonephritis in adults
IgA nephropathy (can present within 5 days of URI or pharyngeal illness)
First step in work-up of confirmed true hypercalcemia?
PTH level
Primary causes of PTH-independent hypercalcemia
- PTHrp (humoral hypercalcemia of malignancy)
- Osteolytic malignancy (e.g. multiple myeloma, breast cancer)
- Hypervitaminosis D (e.g. granulomatous disease, lymphoma, supplementation)
