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
4/n so, we suggest obtaining TEE. However TTE is deemed OK to visualize pulmonic valve. And no fever, no bacteremia thus far, so no TEE…
4/n the next day, pt spikes a fever, the following day, MRSA grows in one (1/6) blood culture. The story starts to build. A kidney biopsy is performed: pauci immune (only 1+ IgM) crescentic necrotizing non-proliferative GN. Morphologically, classic features of ANCA-mimic SBE-GN
5/n so, MRSA coverage is started w/vanco (switched 2 dapto later due to AKI). Cr 3.2-3.4. All good? Wait, Staph-associated infective GNs tend to b IgA dominant, maybe C3 dominant. Pauci immune is <common. On the other hand after, Staph & Strep, 3rd most common bug: Bartonella sp
7/n another look at the #UrinarySediment, RBC casts all over, and waxy casts that seemed to originate from degraded RBC casts, no granular casts.
8/n other RBC casts with fibrinous matrix are also found (see latest @jrseltzer post on @RenalFellowNtwk) and mixed WBC/RBC casts, highly consistent with the subsequent kidney biopsy findings.
9/n I’m itchy. curbsided master diagnostician @martinr43087111 who points out that only 1/6 blood cultures + for MRSA is unusual. Bartonella IgM, IgG and PCR were ordered:
10/n wait, 2 different species growing? Nope, it’s just cross-reactivity. pubmed.ncbi.nlm.nih.gov/8810011/ A repeat TTE is done and reports potential fibrin strands in the pulmonic valve, but not conclusive for SBE. So still not confirmed a source…
11/n any other way to catch the source that it’s not a TEE? 18-F FDG NM PET scan has been described as useful. pubmed.ncbi.nlm.nih.gov/34363148/
12/n so we ordered a FDG PET scan: bright signal detected in the pulmonic valve
13/n Bartonella PCR comes back negative. However, sensitivity of PCR is low and treatment is warranted based on serology and Duke criteria. Doxy + rifampin + CFTX are started
14/n how did the patient get infected? Upon further questioning by medical student @roxnonna23, pt had been exposed with cats with fleas weeks preceding the development of symptoms. Cat lovers, think again
15/n 5/6 blood culture specimens were tossed after 7 days of no growth. There is a reason why Bartonella is known as culture neg SBE. However, our astute ID team ordered more sensitive test for Bartonella DNA (clinicalmetagenomics.org/wp-content/upl…): positive!
16/n pt d/c stable. We hope 4 good progress, learning points:
✅🔬RBC casts/acanthocytes can turn cases 180
✅PR3+ in SBE-GN is not rare➡️ should not lead to AAV IST
✅after Stap/Strep, think Bartonella in SBE-GN
✅Bartonella Ig crossreact
✅Karius > PCR for DNA
✅FDG PET useful
17/17 but perhaps the most important learning point: not settling with an unsatisfactory diagnostic work up is our duty. Be determined and objective to follow the clues. Who will benefit? The patient. @OchsnerNephro
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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.
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
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?