SEVERE ACUTE KIDNEY INJURY WITH SUSPECTED BILATERAL RENAL ARTERY STENOSIS ON RENAL DUPLEX WHILE ON CONCURRENT ACE INHIBITION – A CASE FOR CARBON DIOXIDE RENAL ANGIOGRAPHY

Introduction:

Acute kidney injury (AKI) in the setting of bilateral renal artery stenosis on concurrent ACE inhibition is well described. We describe a 52-year old male hypertensive who developed severe AKI after 9 years on an ACE inhibitor and the renal Duplex examination supported the presence of bilateral renal artery stenosis. We could not get immediate access to carbon dioxide renal angiography to definitely confirm the presence of hemodynamically significant renal artery stenosis. We posit that such patients would benefit from this necessary, effective and non-nephrotoxic diagnostic step.

Methods:

Case report.

Results:

A 52-year-old male with a medical history significant for hypertension and hyperlipidemia, presented to our ED in July 2024 with 6 months of worsening fatigue shortly after treated pneumonia. He experienced progressive weakness, and a 25-lb weight loss and could not get out of bed due to fatigue and poor oral intake on admission day. He had a nonproductive cough and confusion, which started that morning. He disclosed no other symptoms. Two months earlier, he was hypertensive with systolic blood pressure in the 160-180s, and the dose of Lisinopril was increased from 10 mg daily to 40 mg daily and hydrochlorothiazide 25 mg daily was started. He had been on Lisinopril 10 mg daily since July 2015. 

Blood pressure was 107/44, temp 970 F, heart rate 85, RR 18, O2 sats 99% on RA. BMI was 38.4 kg/m2. He was oriented and non-focal. No edema and physical exam was otherwise unremarkable. Pertinent labs - leukocytosis (11.68), hyperkalemia (8.1 mmol/L), metabolic acidosis (bicarbonate 9 mmol/L), BUN 229 mg/dL, creatinine 24.42 mg/dL (baseline creatinine was 1.51 mg/dL on 1/27/2024), phosphorus 12.4 mg/dL, anion gap was 27 mmol/L, eGFR 2 ml/min/1.73 m2, troponin I 0.074 ng/mL, NT proBNP 898 pg/mL, platelet 458 K/cmm and hemoglobin 11.5 g/dL. Urinalysis revealed trace ketones, 1+ blood, 2+ protein and 1+ leukocyte esterase. A1c was 6.6%. Non-contrast head and abd/pelvis CT were negative and showed bilateral nonspecific perinephric edema, without calculi or hydronephrosis. Extensive blood and urine AKI workup including HIV 1 and 2 Ab/p24 Ag, acute Hepatitis panel, were negative including normal total CK and normal serum osmolal gap. Urine tox screen was negative. Ingested volatile alcohols tests were negative. Lactic acid was 1.0 mmol/L. Chest radiograph was normal. Non-contrast head CT showed no evident acute intracranial abnormality. Non-contrast CT abdomen/pelvis revealed nonspecific mild bilateral perinephric edema without calculi or hydroureteronephrosis. Nasal culture was negative. Blood cultures x2 had no growth. 

Lisinopril, Hydrochlorothiazide and Rosuvastatin were promptly discontinued. 

He was making urine and immediate hemodialysis was not indicated. Hyperkalemia was treated with 5 units insulin with IV Dextrose, IV calcium gluconate, 80-120 mg doses of IV Furosemide, repeated every 4 hours and IV fluids containing sodium bicarbonate, 150 mEq in 1000 ml D5W at 200 ml/hour as well as IV Lactated Ringers. A Foley catheter was placed with significant urine output (Figure). In the MICU, he initially required IV norepinephrine pressure support, which was weaned as tolerated. He also received 3 doses of oral sodium Zirconium cyclosilicate, 10 gm, repeated every 6 hours. He promptly responded to therapy with increasing urine output and improving biochemical parameters (Figures). Leukocytosis resolved after one day and he made 1.4 L of urine the first night. He was started on Sevelamer carbonate, taken TID with meals, for hyperphosphatemia and was maintained on a renal diet. 

Renal ultrasound showed right kidney 13.2 cm, left kidney 14 cm, no hydronephrosis but Doppler revealed elevated peak systolic velocities in the proximal right renal artery and mid left renal artery, consistent with bilateral renal artery stenosis. We were unable to carry out carbon dioxide renal angiography to further ascertain the renal artery anatomy without further exposure to potentially nephrotoxic iodinated contrast. Ultrasound-guided left renal biopsy showed acute tubular necrosis, mild thickening of the glomerular basement membranes and early mesangial sclerosis, consistent with early diabetic glomerulopathy, nephrocalcinosis, and mild medial hypertrophy and hyalinosis without necrosis, inflammation or thrombosis of the arterioles. Peak creatinine was 24.42 mg/dL on admission had decreased to 8.26 mg/dL on discharge on hospital day 10. He was discharged on Sevelamer 800 TID with meals, vitamin D supplementation and twice weekly BMP/Phosphorus testing. He was followed in the Nephrology outpatient clinic and 2 months later was back to his usual state of health, normotensive, only on vitamin D supplements and creatinine was normal at 1.20 mg/dL (eGFR=73 ml/min/1.73 m2). We plan to repeat the renal artery Duplex examination.

Conclusions:

We present a case of reversible AKI with life-threatening hyperkalemia and high anion-gap metabolic acidosis in a 52-yo hypertensive male patient who had been on 10 mg daily dose of Lisinopril for 9 years, and who about two months prior to presentation had the dose of Lisinopril increased to 40 mg daily in addition to starting hydrochlorothiazide. He responded to conservative measures. Renal artery Duplex supported the diagnosis of bilateral renal artery stenosis. We could not immediately carry out carbon dioxide renal angiography to ascertain his renal anatomy. We posit that this was a clear medical indication for non-nephrotoxic carbon dioxide angiography. We plan to repeat the renal artery Duplex in the near future.

I have no potential conflict of interest to disclose.

I did not use generative AI and AI-assisted technologies in the writing process.