1/n SIADH is the FSGS of electrolyte disorders. Why? because it represents a pattern of disorder of water regulation (⬆️uOsm, ⬆️uNa) that can be triggered by different mechanisms of disease, like FSGS is a pattern of injury that can be the result of various glomerular hits. 2/n starting with central causes, arginine vasopressin (AVP) increases shortly after subarachnoid hemorrhage (SAH) (PMID 24248182). May also ⬆️ w/cerebral mass/bleed. In experimental SAH, AVP surges right after (PMID 22327731)

1/n Hyponatremia in cirrhosis rounds: case 1: ESLD 2/2 ETOH. Admitted at OUH 2/2 abd distension/lethargy w/sNa 133. Kept on spirono + furosem + lactulose. Gradual ⬇️in sNa in 10 days. Transferred 4 ⬆️level of care. Arrives with sNa 125, sCr 0.8. Alert, jaundice, ascites, no edema 2/n…uNa 48 uOsm 456. No obvious hypervolemia. Dilemma: is uNa not <10 due to ongoing diuretics? History must prevail: exposure to diuretics/laxatives suggest volume depletion factor. Despite high uNa, diuretics are stopped, IV albumin 25 g QID started. 24 hrs later, sNa 129.

1/n new consultation to nephrology: young adult pt arrives to the ED with Na 125, K 2.5, Cl <70, CO2 45, BUN 49, Cr 2.4, Gluc 121. Pt had been hospitalized the month prior with a similar set of labs. At that time Gitelman syndrome was entertained as a diagnosis. 2/n one of the common biases in medicine is anchoring bias. Prior medical records are a common trigger. If it’s written all over the chart, it may get perpetuated unless challenged. So Gitelman was already a favorite here. But let’s learn more about the case…

1/n adult arrives with sudden on onset of weakness, inability to stand. Complaints of muscle tenderness. CPK 11,000. Cr 2.0 mg/dL(baseline 0.9), Phos 7.6. AKI due to toxic ATN/rhabdo. All clear. But, K 2.1 mmol/L! Not the expected hyperkalemia… 2/n immediate reminder that while rhabdomyolysis CAUSES hyperkalemia, hypokalemia may CAUSE hypokalemia: K depletion causes muscle ischemia by preventing normal release of K from myocytes during contraction. Couple of case reports: https://t.co/lNxjqnEnJ2 https://t.co/Qel7WVXH3Ypubmed.ncbi.nlm.nih.gov/24352794/
pubmed.ncbi.nlm.nih.gov/35144389/

1/n young adult presents to the ED with weakness, fatigue & LE edema. Cr 2.8 (base 1.0). Reports tarry stools. Initial clinical impression: ischemic ATN 2/2 GIB. #UrineMicroscopy is performed: crisp RBC casts and acanthocytes are identified in #UrinarySediment. Time to regroup. 2/n pt had a bioprosthetic pulmonic valve from a remote tetralogy of Fallot repair. Radar now centered in the connection between heart valve disease and endocarditis-associated glomerulonephritis (SBE-GN). A transthoracic echocardiogram: no vegetations, no valvular insufficiency

1/n a case of hypomagnesemia: pt sent to clinic 2/2 incidental finding: serum Mg 1.0 mg/dL. Not on diuretics, no diarrhea. Yep, common suspect is present: omeprazole, PPI-induced hypoMg is well-reported. First in 2006, this is an early case series pubmed.ncbi.nlm.nih.gov/20189276/ 2/why do PPIs cause hypoMg?

1/x pt w/o polysubstance abuse, MSSA bacteremia 1-month ago, recent heroin/meth use, arrives to ED with 3 weeks of n/v. Vitals normal. Found to be “dry”. BUN/Cr on arrival 135/23 mg/dL. K 7. Anuric, Foley in. Got IVF boluses, shifted. Not better after that, RRT is ordered. 2/x next am post HD, K better. 5-ml urine are obtained and reportedly showed “ATN” urine, granular casts. A renal US is obtained: Left (“baseline” scan, 11.2 cm), right (new scan, 15.2 cm). Report states no hydro, medical renal dz.

1/11💧 Urine albumin-to-creatinine ratio (UACR) testing in type 2 diabetes (#T2D) – a brief tutorial
👉 What is it?
👉 Why it’s an important complement to eGFR 💉 testing to identify chronic kidney disease (#CKD) in #T2D
COI: #BayerPartner #ItstheKidney ckd-t2d.com 2/11📈UACR estimates 24-hour urine albumin excretion (g/day), assuming that ~1 g of creatinine is excreted in the urine daily.

1/x Pt w/dialysis-dependent AKI arrives from LTAC w/severe acute hypernatremia (166). High GI output is deemed possibly causative. H/o pancreatic/duodenal fístula and PEG. Loss of hypotonic fluids and limited access to water seemed plausible. Let’s look at the rest of the BMP... 2/x the high CO2 (46) suggests met alkalosis. Now, that’s unexpected in a pt with GI losses from supposedly a duodenal fistula. Could he just be a CO2 retainer? Well the ABG confirmed primary met alkalosis. Calculated HCO3 82! That’s a personal record. UOP <400cc/d; no diuretics