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…
4/11 📈Use of UACR to estimate 24-hour urine assessments is supported by longitudinal studies; an example from the Asian Kidney Disease Study (Boon Wee Teo et al 2015; n=232) showed a correlation of r=0.86 between the 2 measures. pubmed.ncbi.nlm.nih.gov/25649135/
5/11 Importantly, a young muscular patient 🏋️♂️ may excrete 2 g/day of creatinine; thus, a UACR of 0.5 g/g would be 1 g/day albumin, not 0.5 g/day. Conversely, a thin older patient 👵 may only excrete 0.75 g of creatinine/day; thus, UACR of 0.5 g/g would be 0.375 g/day.
6/11❔Despite recommendations for annual testing by the American Diabetes Association (ADA), what percentage of patients with #T2D had UACR tests in the ADD-CKD study?
7/11✔The correct answer is (b); only 53% of patients had UACR tests, despite annual testing recommendations by the ADA. Link to the ADD-CKD study here: pubmed.ncbi.nlm.nih.gov/25427285/
8/11 🔽Underutilization of UACR testing is critical, as we know that kidney damage in #T2D, as evidenced by albuminuria (UACR ≥30 mg/g), can occur years ⏰ before impaired kidney function is detected (eGFR <60 mL/min/1.73 m2). (ncbi.nlm.nih.gov/pmc/articles/P…)
9/11 Although this is a known fact, it is important to reiterate that albuminuria (UACR ≥30 mg/g) and impaired eGFR (<60 mL/min/1.73 m2) are also both independently associated with increased mortality in patients with #T2D. (pubmed.ncbi.nlm.nih.gov/23362314/)
10/11 📋 When assessing risk for #CKD, monitoring patients with #T2D at least once a year should include UACR and eGFR. As shown, a patient with eGFR 58 mL/min/1.73 m2 but UACR 700 mg/g is at a greater risk than a patient with eGFR 45 mL/min/1.73 m2 and UACR 50 mg/g.
11/11 👉 Remember, when referring to a patient with #CKD, “baseline eGFR” is only half of the story; the other half should always be “baseline UACR.”
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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?