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Worsening renal failure in older chronic kidney disease patients with renal artery stenosis concurrently on renin angiotensin aldosterone system blockade: a prospective 50-month Mayo-Health-System clinic analysis

M A C Onuigbo, N T C Onuigbo
QJM: Monthly Journal of the Association of Physicians 2008, 101 (7): 519-27
18375475

BACKGROUND: The current US chronic kidney disease (CKD)/end stage renal disease (ESRD) epidemic, coincident with the increasing application of renin angiotensin aldosterone system (RAAS) blockade, has raised concerns of iatrogenic renal failure. The US population is an ageing one, further raising the possibility of increasing renal artery stenosis (RAS) in our patients. Current literature regarding worsening renal failure in CKD patients with RAS is based almost wholly on retrospective studies, and therefore may be poorly understood.

AIM: To prospectively examine the syndrome of worsening renal failure in CKD patients with hemodynamically significant RAS concurrently on RAAS blockade.

DESIGN: Prospective cohort study.

METHODS: Between September 2002 and February 2005, CKD patients, concurrently on RAAS blockade, with RAS >70% by magnetic resonance angiography, who presented with accelerated azotemia (> or =25% increase in baseline serum creatinine) were consecutively enrolled. In addition to standard nephrology care, RAAS blockade was discontinued and renal percutaneous transluminal angioplasty (PTA)/stenting performed according to standard guidelines. Renal function as measured by MDRD-derived eGFR (estimated glomerular filtration rate) was monitored.

RESULTS: Twenty-six Caucasian patients were enrolled-M:F = 10:16, mean age 75.3 years. Prior duration of RAAS blockade was 20.2 months. Known risk factors were absent in 15/26. Unilateral RAS with dual kidneys was common-19/26. Five patients, with higher baseline creatinine-2.1 +/- 0.6 vs. 1.5 +/- 0.4 mg/dl, P = 0.013, progressed to ESRD; 4/5 ESRD patients died after 6.3 months. Excluding the 5 with ESRD, and 2 lost to follow-up, in 19 patients, eGFR increased from 27.8 +/- 9.5 to 39.7 +/- 14.9 ml/min/1.73 m(2) BSA (P = 0.001), 26.4 months after stopping RAAS blockade. In these same 19 patients, mean arterial blood pressure improved from 100 +/- 9 to 92 +/- 10 mmHg, with 8 patients requiring additional antihypertensive substitutions. Renal PTA/stenting further improved eGFR in 7/9 patients.

CONCLUSION: Contrary to previous retrospective reports, we observed that renal failure/ESRD in this older CKD patient population is common in patients with unilateral RAS lesions with dual kidneys; precipitating risk factors are often absent, and progression to ESRD with increased mortality is not infrequent. Older age, higher baseline creatinine (>2.0) and/or lower eGFR (<35) predicted ESRD. eGFR improved following discontinuation of RAAS blockade, generally. Furthermore, in selected patients, renal PTA and stent placement led to additional improvements in eGFR. Our observations call for further studies.

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