Over the last month, I’ve picked up a lot of factoids on the renal consult service which I’d like to brain dump for future reference:
- When it comes to measuring proteinuria, a spot protein/creatinine ratio is a reliable alternative to more cumbersome 24-hour urine total protein (UTP) in chronic renal disease patients (including those with diabetes and lupus nephritis).
- Excessive abdominal pressure (ie, massive volume of cirrhotic ascites) can essentially “crush” the kidneys and produce a decrease in effective circulating volume leading to a pre-renal state. Look out for this in recent abdominal surgeries and patients requiring paracenteses. Get a bladder pressure and tap the fluid.
- C4 is decreased in cryoglobulinemia (think hepatitis C)
- Acanthocytes in the urine point toward a glomerular injury.
- A five day course of prednisolone (35mg/day) has equal efficacy to five days of naproxen (500mg BID) in treating acute gout flares.
- For any patient with an acute kidney injury (AKI), hold their ACE inhibitor and diuretics.
- Fleet enemas (sodium phosphate) are not indicated in CKD patients. Phosphates can go sky high… raising the concern for phosphate nephropathy.
- The calcium-phosphate product should be maintained below 55. Otherwise, there’s a risk for calcium phosphate precipitation.
- Cardiorenal diseases gives a pre-renal picture with no response to fluids. The drop in cardiac output “shocks” the highly vascular kidneys – diuresis and ionotropes can improve the pump.
- Differential for large kidneys: HIV-associated nephropathy (HIVAN), diabetes, a solitary kidney with compensatory hyperfiltration, polycystic kidney disease, and a myriad of infiltrative diseases (multiple myeloma, amyloidosis, etc.)
- Solitary kidneys can undergo secondary focal segmental glomerulosclerosis (FSGS) from chronic hyperfiltration.
- A creatinine of 1 is not normal in patients with amputations, especially those involving the large muscle groups of the lower extremities.
- Because of variable electrolyte diuresis on diuretics, the fractional excretion of sodium (FENa) is not a reliable. Use the fractional excretion of urea instead.
- Immunosuppresants predispose patients to malignancies which, in turn, can lead to membranous nephropathy.
- Primary FSGS involves a full blown, idiopathic, diffuse effacement of podocytes leading to heavy proteinuria. Treatment typically focuses on prednisone or other immunosuppressive modalities. Secondary FSGS is more insidious as some glomeruli are spared of podocyte effacement. Treatment involves blood pressure control (typically with an ACE inhibitor).
Two more days on this rotation and then it’s off to the progressive care unit (PCU) at Texas Children’s Hospital! 🙂