Nephrology Flashcards
First Aid and NEJM Knowledge+
Rate by which to raise Na in acute vs. chronic symptomatic hyponatremia
Acute symptomatic (seizing!?): raise until symptoms resolve 1-2 mEq/L/hr
Chronic symptomatic: slower raise, 0.5-1.0 mEq/L/hr
Clinical features of hyponatremia
Symptoms typically correlate to rate and severity of decline
Seizure, coma
AMS- confusion, lethargy
Nausea/vomiting
Overcorrection of hyponatremia raises risk for what?
Overcorrecting hyponatremia (raising blood Na too fast- drawing water out of brain) => CPM (central pontine myelinolysis)
Do not correct Na by more than 10-12 mEq/L over 24 hrs
Overcorrection of hypernatremia raises risk for what?
Cerebral edema- drop sodium fast, water goes into brain
Main three causes of SIADH
- CNS pathology: SAH, subdural, meningitis, tumor, CVA
- Pulmonary: SCLC, Tb, pneumonia
- Drugs: typically psychotropic meds (TCAs, haldol, SSRIs)
Urine osmolality in SIADH vs. psychogenic polydipsia
SIADH- high urine osms (over 100, UNa over 20) b/c body holding onto water
Psychogenic polydipsia- low urine osms (below 50) b/c body trying to get rid of as much water as possible
Prototypical clinical vignette for hypernatremia
Hypernatremia- due to hypovolemia (almost always from free water deficit and not due to high salt)
Old demented bedridden pt who can’t get up and respond to thirst reflex
When to think of diabetes insipidus in hypernatremic pt
DI = either not producing (central) or not responding to (nephrogenic) ADH => have dilute urine despite hypernatremia
So when hypernatremic with Uosm low consider DI
Name a cause of hypervolemic hypernatremia
Rare that hypernatremia is in s/o hypervolemia- consider primary hyperaldosteronism = mineralocorticoid excess (aldo prompts holding onto Na)
Name causes of hyperkalemia due to extracellular K+ shift
K+ pushed out of cells metabolic acidosis (ex: DKA) tumor lysis rhabdo digitalis overdose
EKG changes of mild, moderate, severe hyperkalemia
Mild- normal, peaked T-waves
Moderate- (pulling the string)- prolonged QRS, flattened P-waves
Severe- VF
Mechanism of type I (distal) RTA
Distal RTA due to inability to secrete acid load in distal part of nephron (collecting duct)
Most commonly due to reduced activity of H/K ATPase that secretes H+ ions => also results in hypokalemia (b/c K left in urine)
Mechanism of type II (proximal) RTA
Proximal inability to reabsorb bicarb => lose bicarb in urine
2 main etiologies of non-anion gap metabolic acidosis
(a) How to distinguish
Non-anion gap metabolic acidosis due to loss of bicarb containing solutions (from kidneys (type II RTA) or GI (diarrhea)) or inability to excrete H+ (type I RTA)
- Diarrhea
- RTA
(a) Clinically (duh) and also by urine anion gap
if positive urine AG then RTA present
Type I (distal) RTA
(a) Clinical distinguishing feature
Type I RTA = inability to secrete H+ ions into urine => hypokalemia and metabolic acidosis
(a) often presents w/ recurrent kidney stones or hypercalciuria
- acidemia increases CaPO4 release from bone during buffering
- alkaline urine promotes stone formation
Causes of type II (proximal) RTA
Proximal RTA (type II) = bicarb wasting- means that the bicarb filtered can’t be reabsorbed in the proximal tubule
Causes
M-protein disorders: multiple myeloma, amyloid
Heavy metal poisoning: Pb, Cu
Acetazolamide
Liddle syndrome
Liddle syndrome = psudeohyperparathyroidism- autosomal dominant mutation in ENac that mimics high aldo b/c increased Na reabsorption and decreased K reabsorption =>
refractory HTN and hypokalemia, and metabolic alkalosis
Bartter’s vs. Gitelman’s syndrome
Both autosomal recessive genetic defects that cause hypokalemia and mimic loop diuretic (Barter’s) and thiazide diuretic (Gitelman’s) use
Differentiate by urine Ca
Bartter’s- high urine Ca
Gitelman’s- low urine Ca
Name some etiologies of renal K+ loss (hypokalemia due to something at level of kidney)
Diuresis Mineralocorticoid excess: licorice, Hyperaldo, Cushing's disease- at high levels cortisol has mineralocorticoid properties Liddle syndrome (pseudohyperaldo due to genetic ENac mutation)
Etiologies of type I RTA
Type I (distal) RTA = inability of kidney to secrete acid in collecting duct
Main causes
- Sjogrens
- amphotericin
Two main ways by which kidneys maintain acid/base status
- Reabsorption of bicarbonate that is filtered into the proximal tubule
- Secretion of daily acid load (from sulfur-containing amino acids) in collecting duct
Mechanism of hypokalemia in type I (distal) RTA
Distal RTA = reduced ability to excrete H in collecting system
Renal potassium wasting- b/c H/K ATPase isn’t doing its thing to pump out H and bring in K
- diminished H-ATPase activity is the most common cause of distal RTA
Main cause of type IV RTA
Hypoaldo => hyperkalemia and metabolic acidosis
Explain concept of delta-delta (or delta gap)
Delta gap- use this when you have an anion-gap metabolic acidosis to see if there is a concomitant non-anion-gap metabolic acidosis present
If (AG - 12) / (24 - bicarb) is less than one: suggests presence of concomitant non-anion gap metabolic acidosis
D/D over 2 c/w concomitant metabolic alkalosis (HCO3 much higher than expected for degree of acidosis)
On an ABG once you find an anion-gap metabolic acidosis, what are the two next steps
- Check delta-delta to see if concomitant non-anion gap metabolic acidosis is present
- Use winter’s formula pCO2 = (HCO3 x 1.5) + 8 +/- 2 to check for adequate respiratory compensation
Explain rationale behind winter’s formula
Winter’s formula- used to calculate respiratory compensation for metabolic acidosis
pCO2 = (HCO3 x 1.5) + 8 +/- 2
If pCO2 is over expected value- concomitant respiratory acidosis
if pCO2 under expected value- concomitant respiratory alkalosis
Lab tests to distinguish three main types of RTA
Hyperkalemia = type IV RTA
Hypokalemia or normkalemia seen in type I and type II, to differentiate use urine pH
Urine pH over 5.5 = distal (type I) RTA
Urine pH under 5.0 = proximal (type II) RTA
Degree of low bicarb
Lowest in type I (distal)
Moderately low in type II (14-20)
Usually over 15 in type IV
Other lab findings typically found in type II RTA
Any cause of type II (proximal) RTA can also cause Fanconi’s syndrome where nothing gets reabsorbed proximally => hypophosphatemia, glycosuria despite normal serum glucose, low-grade proteinuria
Bicarb compensation for acute vs. chronic respiratory acidosis
Respiratory acidosis (pCO2 over 45)
For every 10 mmHg increase in pCO2
- acute: 1 mEq/L raise in bicarb
- chronic: 3-5 mEq/L raise in bicarb
Bicarb compensation for acute vs. chronic respiratory alkalosis
Respiratory alkalosis (pCO2 under 35)
For every 10 mmHg decrease in pCO2
- acute: 2 mEq/L drop in bicarb
- chronic: 4 mEq/L drop in bicarb
Which acid base disturbances are present 27 y/oF w/ type I diabetes p/w intractable vomiting/abdominal pain
pH 7.52, pCO2 30, pO2 260 on RA
AG 40
Bicarb 15
Mixed:
- anion-gap metabolic acidosis (probs from DKA)
- delta/delta = (40-12) / (24-15) > 2 c/w concomitant metabolic alkalosis (likely from the vomiting)
- Compensatory respiratory alkalosis
What acid/base disorder is caused by salicylate toxicity
Triple
Anion-gap metabolic acidosis (from the salicylic acid), metabolic alkalosis (from vomiting) and primary respiratory alkalosis (salicylate directly stimulate the respiratory center causing tachypnea)
Typical clinical presentation of nephrolithiasis
(a) UA findings
Kidney stones typically present w/ flank/back pain radiating to the groin
Also often w/ cystitis features of frequency, dysuria, urgency
(a) Hematuria on UA (at least 10 RBCs)
Most common form of kidney stones
(a) Other types
Calcium oxalate stones account for about 80% of kidney stones
(a) Other types include uric acid stones, struvite stones, and cysteine stones
Utility of AXR in finding kidney stones
(a) Gold standard diagnostic imaging
KUB can see calcium oxalate stones (most common type) but miss uric acid stones
(a) Gold standard is non-con abdominal CT
3 types of urine abnormalities that increase risk of calcium oxalate kidney stones
Increase risk of calcium oxalate kidney stones
- Hypercaliuria seen in hyperparathyroidism
- Hyperoxalaturia seen in short-gut syndrome/IBD
- Hypocitraturia seen in metabolic acidosis (RTA, CKD, chronic diarrhea)
2 types of urine abnormalities that increase risk of uric acid kidney stones
Increased risk of uric acid kidney stones
- Acidic urine (pH below 5.5): diets high in animal protein (b/c urine excretes daily H+ load from sulfur-containing amino acids
- Hyperuricosuria: gout, tumor lysis syndrome
Medical treatment of calcium oxalate kidney stones
Calcium restriction does NOT help b/c can lead to hyperoxaluria (calcium binds oxalate in the gut to promote excretion)
- tons of PO hydration
- thiazides (reduce Ca excreted in urine)
- K citrate
Type of kidney stone more likely to be seen in acidic vs alkaline urine
Acidic urine (pH under 5.5) predisposes to uric acid kidney stones
Alkaline urine (pH over 6.5) predisposes to struvite stones
The following clinical history increases risk of which type of kidney stone
(a) Recurrent UTI
(b) Malignancy in current treatment
(c) IBD
(a) Recurrent UTIs w/ urease producing organisms increases risk for struvite stones
(b) Consider tumor lysis syndrome => hyperuricosuria => uric acid kidney stone
(c) IBD predisposes to hyperoxaluria (b/c oxalate excreted by gut) which increases risk of calcium oxalate kidney stones
2 conditions that make checking a FeNA useless
- Pt on diuresis
2. Pt not oliguric!!! Remember FeNa is only of use if the pt is oliguric
Urine osmolality expected in
(a) Prerenal azotemia
(b) ATN
Urine osms in
(a) Prerenal azotemia- very high osms, urine concentrated b/c kidneys are functionally able to hold onto water
(b) ATN- usually similar to plasma, intrinsic kidney issue so that tubules cannot concentrate
UA findings (casts/cells) seen in the following causes of acute renal failure
(a) Pre-renal
(b) Atheroembolism to renal artery
(c) ATN due to ischemia
(d) AIN from drug
UA findings
(a) Pre-renal: low SG, nonspecific hyaline casts
(b) Atheroembolism: eosinophiluria (eos in urine)
(c) ATN from ischemia (ex: sepsis, shock)- muddy brown casts
(d) AIN from drug or contrast- white cell casts
Key diagnoses for the following clues on UA
(a) Muddy brown casts
(b) Dysmorphic RBCs and RBC casts
(c) WBC casts
(d) Hyaline casts
UA findings
(a) Muddy brown cast = ATN, typically from ischemia (ex: ATN after bout of sepsis)
(b) Dysmorphic RBC/RBC casts seen in glomerulonephritis/vasculitis
(c) WBC casts seen in AIN in response to contrast or nephrotoxic drugs
(d) Hyaline casts are nonspecific, can be seen in dirty UAs or pre renal azotemia
Treatment options for HRS before liver transplant
- albumin
- splanchnic vasoconstrictors = vasopressin analogus = octreotide, midodrine
- TIPS
- RRT as bridge to transplant
27 y/oF w/ worse HTN after starting ACEi
Next best test
Renal artery duplex to assess renal artery flow- worsening of HTN after initiation of ACEi is suspicious for renovascular HTN (ex: renal artery stenosis in s/o fibromuscular dysplasia?
Urge incontinence vs. stress incontinence
Urge incontinence = overactive bladder, feel the need to go right before involuntary leakage of urine
Stress incontinence = involuntary leakage w/ increases in abdominal pressure (sneezing, vagal maneuver)
Urge incontinence vs. stress incontinence
Urge incontinence = overactive bladder, feel the need to go right before involuntary leakage of urine
Stress incontinence = involuntary leakage w/ increases in abdominal pressure (sneezing, vagal maneuver)
Elderly M w/ post-renal obstruction 2/2 prostate requiring foley: start on finasteride or tamsulosin
Tamsulosin (alpha blocker) in acute setting b/c finasteride (PDE5 inhibitors take weeks to kick in)
Acid/base disturbance seen in aspirin toxicity
Elevated salicylate level => primary respiratory alkalosis w/ secondary metabolic acidosis
When is EPO indicated in ESRD?
EPO indicated when Hb under 10 despite adequate iron stores
EXCEPT in cancer pts, actually increases risk of tumor progression
So cancer pt w/ ESRD and Hb 8- give IV Iron, NOT EPO
Workup of painless hematuria in 65 y/o smoker
Need to evaluate both upper and lower GU tract for cancer
- CT urography to look for RCC, urolithiasis, ureteral mass/stone (CT urogram w/ contrast, better than IV pyelogram)
- Cystoscopy for bladder CA
