Macaulay A C Onuigbo1, Nnonyelum T C Onuigbo. 1. Department of Nephrology, Midelfort Clinic, Mayo Health System, Eau Claire, WI 54702, USA. onuigbo.macaulay@mayo.edu
Abstract
BACKGROUND: Worsening azotemia following initiation of angiotensin blockade (AB), in patients with CKD, RAS with/without precipitating factors is recognized. Small increases in serum creatinine following initiation of AB occur and must not warrant drug discontinuation. We anecdotally had observed improvement in CKD in patients with normal renal arteries and no precipitating factors, following termination of AB. The worldwide ESRD epidemic, coincident with increasing use of AB, prompted us to hypothesize a late-onset azotemia in such CKD patients. MATERIAL/ METHODS: Over 30 months, 103 patients with worsening azotemia, while on AB were evaluated. Ninety-seven patients with abnormal MRA and/or with precipitating factors were excluded. In the remaining five, AB was discontinued, and GFR monitored. RESULTS: One male, four females, mean age 66.2 years. Three diabetic/hypertensives, one SLE/hypertensive, one diabetic/kidney transplant recipient. Mean stable AB, 25.2 months, (6-66 months). Mean follow up, 11.8 months. One month following discontinuation of AB, GFR increased by a mean 45%. Mean serum creatinine decreased from 2.9+/-0.9 to 1.8+/-0.4 mg/dL (p=0.04). Uremic symptoms in 3, hyperkalemia in one, secondary hyperparathyroidism in one, resolved. Two with anemia, now require less erythropoietin. CONCLUSIONS: We called this unrecognized potentially reversible late-onset worsening azotemia, occurring several months to years on stable AB, in CKD patients with normal renal arteries, without precipitating factors, late-onset renal failure from angiotensin blockade (LORFFAB). Pathophysiologically, the concept of microvascular RAS is invoked. The extent of LORFFAB, with millions of patients worldwide on AB, remains conjectural and warrants further investigation.
BACKGROUND: Worsening azotemia following initiation of angiotensin blockade (AB), in patients with CKD, RAS with/without precipitating factors is recognized. Small increases in serum creatinine following initiation of AB occur and must not warrant drug discontinuation. We anecdotally had observed improvement in CKD in patients with normal renal arteries and no precipitating factors, following termination of AB. The worldwide ESRD epidemic, coincident with increasing use of AB, prompted us to hypothesize a late-onset azotemia in such CKDpatients. MATERIAL/ METHODS: Over 30 months, 103 patients with worsening azotemia, while on AB were evaluated. Ninety-seven patients with abnormal MRA and/or with precipitating factors were excluded. In the remaining five, AB was discontinued, and GFR monitored. RESULTS: One male, four females, mean age 66.2 years. Three diabetic/hypertensives, one SLE/hypertensive, one diabetic/kidney transplant recipient. Mean stable AB, 25.2 months, (6-66 months). Mean follow up, 11.8 months. One month following discontinuation of AB, GFR increased by a mean 45%. Mean serum creatinine decreased from 2.9+/-0.9 to 1.8+/-0.4 mg/dL (p=0.04). Uremic symptoms in 3, hyperkalemia in one, secondary hyperparathyroidism in one, resolved. Two with anemia, now require less erythropoietin. CONCLUSIONS: We called this unrecognized potentially reversible late-onset worsening azotemia, occurring several months to years on stable AB, in CKDpatients with normal renal arteries, without precipitating factors, late-onset renal failure from angiotensin blockade (LORFFAB). Pathophysiologically, the concept of microvascular RAS is invoked. The extent of LORFFAB, with millions of patients worldwide on AB, remains conjectural and warrants further investigation.