An elderly male w/ history of MCD on chronic cyclosporine with good response, presents with subacute weakness and fatigue found to have AKI (Cr to 7 up from ~2.5). Initially the cause of AKI was unclear and he was given gentle fluids overnight; it now seems that the etiology is relapse of MCD + Cyclosporine toxicity.
When do you give bicarb for metabolic acidosis in renal failure?
*The treatment of severe acute metabolic acidosis is controversial; though there are some concerns about myocardial depression and vasodilatory collapse at extreme low pHs, the data in human subjects is poor. Overall, most clinicians consider initiating treatment of metabolic acidosis when pH < 7.1.
*Because bicarb is actually converted to CO2, use caution about giving this when acidosis is severe. In these cases, and in cases when you must avoid a sodium load, you can consider using THAM (tromethamine) as an alternative buffer. THAM cannot be used in renal failure.
*Bicarbonate supplementation is recommended for all patients with CKD + metabolic acidosis to maintain a goal bicarb of >22. This is based on RCTs showing benefits in terms of a) progression of CKD, b) bone health, and c) nutritional status. See below for one of the landmark trials of this published in 2009.
A young man with a pmh of anxiety who presented with lower extremity numbness and weakness after being down for several hours. Further workup revealed severe transaminitis as well as AKI and an elevated CK consistent with rhabdomyolysis. His UTox was positive for meth, which helped further explain his presentation.
-Hypovolemia, Metabolic Acidosis, Hyperthermia, and Rhabdomyolysis occur in a LARGE number of meth cases. Workup for suspected meth intoxication should include: serum electrolytes, lactate, CPK, ALT/AST, clotting times, and renal function – this patient had significant LFT derangements as well as rhabdo
-Rectal administration of meth is referred to as “booty bumping”
-Among patients with rhabdomyolysis, fluid repletion should be continued until plasma CK levels decrease to <5000 unit/L and urine is dipstick negative for hematuria
A middle aged man w/ IVDU, HCV presented with worsening recurrent edema, found to have nephrotic syndrome.
Mnemonic for remembering low-complement glomerular disease: “C-LESS”
Cryoglobulins (+other types of MPGN which is the histologic dx for cryo)
Staph and Strep infections
Treatment of HCV-mediated cryoglobulinemia:
-All patients should be treated with antivirals for HCV
-There are specific indications for the addition of immunosuppression, including rapidly rising creatinine AND nephrotic range proteinuria (rituximab is usually first line though prednisone can also be used)
An older female w/ HCV p/w shortness of breath and volume overload, found to have proteinuria, hyertension, and hypoalbuminemia. Urine sediment showed dysmorphic reds, and complement levels were low. The diagnosis of GN with nephrotic features was made, thought likely 2/2 MPGN given her history of untreated HCV and complement levels; final results of a renal biopsy are pending.
Main Teaching Point:
Nephritic/Nephrotic syndromes represent a spectrum of disease. The syndromes that most often present with both nephrotic and nephritic features include MPGN, membranoproliferative glomerulonephropathy, and lupus nephritis. Generally, the mixed syndromes are the most severe – exceptions include RPGN (mostly nephritic) and HIV nephropathy, which both can quickly progress to ESRD.
*When you want to estimate CVP and can’t see the IJ:
-The EJ has been validated as a reliable surrogate (Vanayak AG et al. “Usefulness of the external jugular vein examination in detecting abnormal central venous pressure in critically ill patients”. Arch Intern Med 2006.)
– Hand raise (watch for hand veins to flatten as you lift arm towards heart level)
– Ultrasound to look at IJ or IVC