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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1/11💧 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#ItstheKidneyckd-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.
3/11 An important paper by @NephRodby shows the usefulness of urine protein-to-creatinine ratio (UPCR) in predicting 24-hour protein excretion while critically assessing the values at hand. ajkd.org/article/0272-6…
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
3/x a logical hypothesis was high output from PEG to suction. Not the case. Pt being fed 4 comfort ~ 1 L/day. But output from enteric fistula was 3-4 L/day. Upon reading Surg report, there was a note about a jejunal “hole”. Does it matter if fistula is duodenal, ileal or jejunal?