Nephrology Flashcards
Acid urine pH
High protein diet
Increases risk for uric acid stones
Type IV distal RTA
High urine PH
Urease-splitting organisims (proteus), type I and II RTA, increased risk for struvite stones
Primary protein checked by dipstick
Albumin
Positive ketones on dipstick
DKA, starvation ketoacidosis, vomiting, pregnancy
Glucosuria in the absence of serum hyperglycemia
Indicates proximal tubule dysfunction (myeloma, drug exposure, Fanconi syndrome)
Reasons for negative urine nitrite in UTI
Nonconverting organisms like (Enterococcus, Staphylococcus, Streptococcus, Haemophilus_
Conditions that cause calcium phosphate crystals
Distal RTA, tumor lysis syndrome (also causes uric acid crystals)
Evaluation of hematuria in patient older than 35
CT urography or noncontrast, helical CT if stone suspected
Bladder US is reasonable if wanting a cheap and fast screen but gold standard is above
If negative, cystoscopy is needed
Best test for renal artery stenosis other than doppler
MR angiography (can even get without contrast if really needed)
Test for urinary potassium losses
Spot K+/Cr ratio: <13 indicates hypokalemia due to lack of intake or GI losses
Otherwise, consider other causes like aldosteronism, diuretic use, RTA, Barter/Gitelman (diuretic mimicry)
Causes of hypophopshatemia
Refeeding syndrome Insulin treatment Respiratory alkalosis Meds (calcium, antacids) Diarrhea/renal wasting (>100mg/24hrs or check FEPo4 with MD calc) Hyperparathyroidism
Newly identified cause of hypomagnesemia
Prolonged use of PPIs
Causes of hypomagnesemia
Diuretics Cisplatin, calcineurin inhibitors VEGF inhibitors Alcoholism Volume expansion DKA
For what acid-base disorder is Winter’s Formula used?
Metabolic acidosis
1.5(HCO3) + 8 +/-2
Gives you the expected pCO2
Treatment of alcoholic ketoacidosis
IV saline AND D5w; need insulin secretion and suppression of glucagon release
Make sure to give thiamine prior to starting
Treatment goal for salicylate toxicity
NaHCO3 w/ goal urine pH 7.5
Urine anion gap uses and components
Used to differentiate normal anion gap acidosis and need a urine Na, K, and Cl
Positive = RTA Negative = Diarrhea
Type II RTA
Proximal tubule fails to resorb HCO3 leading to acidosis
Can have acidic urine still since distal nephron is still intact
Tx: Alkalinize the urine; consider thiazides
Fanconi Syndrome
Glycosuria, phosphaturia, aminioaciduria, hypouricemia all due to failure of the proximal renal tubule
Usually associated w/ Type II RTA
Type I RTA
Failure of DCT to secrete H+
Known causes include lithium, Wilsons, dysproteinemias
Associated with urinary potassium wasting and hypocitraturia which predisposes to renal calculi
Tx: Potassium citrate
Type IV RTA
Caused by aldosterone deficiency or resistance seen with diabetic nephropathy (due to hyporeninism), ACEi/ARB, heparin, and COX-2 inhibitors
Tx: Underlying cause; can consider fludrocortisone, thiazides, loop diuretics
Patient not on diuretics but has metabolic alkalosis and high urine chloride
Consider Bartter and Gitelman syndromes
Timing of rise in creatinine with aminoglycosides
5-7 days after initiation
Can also see loss of pretty much all electrolytes
Cisplatin induced AKI
Directly nephrotoxic and also causes renal vasoconstriction
Hypomagnesemia w/ urinary wasting of magnesium is common
Goals for treatment in pigment related AKI
Fluid resuscitate w/ goal UOP 200-300cc/hr
Additionally, could alkalinize the urine if no improvement to prevent cast formation, however, if patient becomes hypocalcemia or alkalotic, may need to discontinue
Acute interstitial nephritis w/ NSAIDs or PPI
Classic triad of fever, rash, and eosinophilia is rarely ever present with these two common medications
Labs to check w/ AMS and history is suggestive of ingestion
HCO3, serum osmols and osmol gap, urine osmol gap, UA for crystals (calicum oxalate w/ polyethylene glycol or excessive orlistat)
Complication with peritoneal dialysis
Peritonitis; will lead to fibrosis and make PD ineffective
Med classes renal transplant patients need to be one
Calcineurin inhibitors (tacrolimus, cyclosporine)
Antimetabolites (Mycophenolate or Azathioprine)
Glucocorticoids
Most common intrinsic renal kidney disease to occur post transplant
FSGS
Cancers most common in renal transplant patients
Non melanoma skin cancer
Kaposi sarcoma
Lymphoproliferative cancers
FSGS pathologic mechanism
Immunologic injury from leukocytes producing a factor that directly targets podocytes causing glomerular detachment; associated w/ APOL1 gene in african americans and obese people
Leading cause of nephropathy in white people
Membranous nephropathy
Clinical presentation of membranous nephropathy
Slowly progressive edema w/ labs showing nephrotic stuff, however, renal fnxn remains mostly intact (as opposed to FSGS)
Patient’s are also more prone to thrombotic complications, especially when albumin <2.8
What should you consider when a patient is diagnosed w/ membranous nephropathy?
Possibility of cancer; malignancy detected in 25% of patients within 1 year of diagnosis
Perform age appropriate screening
Most common glomerular disease worldwide
IgA nephropathy
IgA nephropathy pathology
Deficient IgA1-producing cells cause galactose deficient IgA to be attack by antibodies and form deposited immune complexes producing microscopic/gross hematuria or can become more aggressive and look like a traditional glomerulonephritis
Tubloreticular inclusions in glomerular endothelial cell cytoplasm on EM of kidney biopsy
“interferon footprints”
*pathognomic for lupus nephritis
Membranoproliferative glomerulonephritis classic association?
Hepatitis C
