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.
3/x before the US, cognitive bias may lead to conclude early that we were dealing with just a bad ATN, not unreasonable in a pt who vomited and consumed drugs for several days. However, nephromegaly and remarkable ⬆️parenchymal echogenicity seems out of proportion for just an ATN
4/x so, additional 5-ml of urine are obtained. At LPF, there’s a general “ATN” sediment with a few dark casts here and there
5/x however, at HPF, the truth is revealed: RBC casts are found in fair number (btw, lab later reported hyaline/granular) #UrinarySediment
6/x many pigmented (hem) waxy casts are also found, along with dysmorphic RBCs (not quite acanthocytes). So, definitely pointing to acute GN and concomitant tubular injury #UrinarySediment
7/x so at this point, the h/o MSSA became extremely important, suspicion of infection-related GN must be considered. That day, low grade fever developed. Of course, next step is to get an echocardiogram. Boom, vegetation.
8/x SBE-GN can lead to crescentic pauci immune or crescentic DPGN. C3 low in ~50% (normal here), +MPO-ANCA (pending here). Back on cefazolin. CT Sx consulted. Kidney biopsy scheduled. We may see this lesion 👇
9/9 conclusions: 1. Important to avoid cognitive (confirmation) biases; 2. #UrineMicroscopy is a valuable tool; 3. Kidney US is not just to r/o hydro, check size, echogenicity; 4. IVDA+bacteremia+AKI: think SBE-GN
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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)
3/n Pain is a known stimulus for serotonin. SSRIs are arguably the most common drugs linked to SIADH (carbamazepine > risk but less commonly used). Intracerebroventricular serotonin infusion led to brisk ⬆️AVP in a rat model (PMID 12588512). More studies needed in this area.
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.
3/n spironolactone effect doesn’t go away fast. It’s a long acting drug. Plus, CCD cells need to recover from MR antagonism, synthesis and cell membrane insertion of new ENaC subunits takes some time. So, don’t expect uNa to turn <10 the next day, especially if volume is given
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…
3/n pt had presented to the ED complaining of weakness, tremors and nausea and vomiting for the last week or so. No prior medical hx. No meds. BP 135/90, otherwise normal vitals. Unremarkable exam. IV 0.9% NaCl and KCl are started. ABG: 7.56/57/45. Pure metabolic alkalosis
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/
3/n the next question in this case was why was the pt so profoundly hypokalemic? Hypokalemic paralysis quickly calls for mutation periodic paralysis (rare) and distal RTA from Sjogren/RA (not so rare). Just one case here pubmed.ncbi.nlm.nih.gov/35242331/
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
3/n as part of the nephritic work up, PR3 returns with low titer positivity. Primary AAV? Actually, that finding strengthened the case for SBE-GN since it’s known that 20-40% of them are PR3+ link.springer.com/content/pdf/10… this @arkanalabs@renalpathdoc review is a must read
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?
3/n turns out that the same Mg channel TRPM6 that is expressed in the DCT is also expressed in the gut. Top 2 panels are colon & duodenum. Bottom right is DCT.