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 21^st 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 a component of physical examination in any patient with AKI. Ideally, it must be performed as soon as the AKI is diagnosed rather than waiting for specialty referral or radiology appointment. It is possible that our patient would have had better renal recovery if the ultrasound was performed and acted upon when the initial drop in renal function was noted.

• Obstructive nephropathy doesn’t necessarily present with classic symptoms and signs.

• Don’t always blame the diuretic for AKI. It is unfortunate that many physicians consider diuretics to be ‘nephrotoxic’ agents. In reality, if the patient is prone to congestive nephropathy (underlying heart failure or other fluid overload states), discontinuing diuretics without physical examination (POCUS) often does more harm than good.