An elderly gentleman was seen in the nephrology clinic for acute kidney injury (AKI) on underlying chronic kidney disease stage III. Estimated glomerular filtration rate (eGFR) was 18 ml/min at presentation. It was 30 ml/min 3 months prior to that and 52 ml/min a year ago. He was on a small dose of loop diuretic for pedal edema, and it was discontinued by the primary care provider when the eGFR dropped to 30. However, as the renal function continued to worsen, he was referred to nephrology. The patient was asymptomatic at presentation except for mild pedal edema. Systolic blood pressure was ~165 mmHg. There were no urinary complaints suggestive of infection or obstruction. On repeated questioning, the patient joking said, “of course, my urine stream is not so great as that of a 20-year-old”. After careful history taking and conventional physical exam, there was no obvious cause of AKI identified. Logical next step? Physical examination of the 21st century using POCUS. I hope you remember how we perform POCUS-assisted physical examination in AKI. If not, have a glance at this article.
On examination (POCUS), there was no significant extravascular lung water except for occasional B-lines at bases, left ventricular systolic function was preserved, no gross right ventricular dilatation, inferior vena cava was approximately 1.9 cm with less than 50% inspiratory collapse suggestive of intermediately elevated right atrial pressure and portal vein Doppler flow was continuous. So, there was no sonographic evidence of congestive nephropathy, though the patient was mildly hypervolemic. Now we take a look at the kidney and find bear paws bilaterally! (Severe hydronephrosis). Bladder appeared super full. No obvious intra-luminal abnormalities noted in the bladder. Strangely, patient was not feeling the urge to urinate.
Asked the patient to go to the bathroom and try to urinate. While he thought he “urinated quite a bit”, repeat bladder scan was essentially similar to the one performed pre-void (see below). It’s difficult to measure the exact volume as the walls are not completely visualized in one frame. However, it doesn’t matter; patient has significant bladder outlet obstruction leading to obstructive nephropathy.
Patient was sent to the emergency room where placement of a Foley catheter returned over 6 liters of urine. Seen by urology and discharged with indwelling urinary catheter and an appointment for urodynamic studies. At the time of 4-week follow up in the nephrology clinic, patient was feeling fine, serum creatinine trended down and the eGFR was approximately 39 ml/min. Interestingly, the systolic blood pressure was in 130s without any medication changes. It is known that urinary obstruction leads to elevated blood pressure. Repeat kidney and bladder ultrasound images shown below (hydronephrosis resolved; bladder decompressed with Foley catheter).
Teaching points:
- Kidney ultrasound is part of the physical exam. Don’t delay it: In any patient with AKI, kidney POCUS should be considered an essential component of the initial evaluation. It should not be postponed until a specialty referral or radiology appointment becomes available. In some cases, early imaging might have altered the course and improved renal recovery if done and acted upon when the initial decline in kidney function was noted.
- Obstruction doesn’t always come with textbook symptoms: Obstructive nephropathy can be surprisingly subtle. Classic signs like lower urinary tract symptoms or flank pain may be absent. If the clinical picture feels off, keep obstruction in the differential even when obvious symptoms are missing.
- Stop blaming the diuretic. Start examining: The idea that diuretics are inherently nephrotoxic is widespread but often misguided. In patients vulnerable to fluid overload, such as those with heart failure, stopping diuretics without proper assessment can be harmful. A focused clinical evaluation using POCUS, is essential before making that decision.