What question did this study set out to answer?

To evaluate whether patients with chronic kidney disease on long-term RAAS blockade can develop delayed azotemia despite having normal major renal arteries and no precipitating triggers.

January 1, 2008Renal FailureOpen Access

Late Onset Azotemia from RAAS Blockade in CKD Patients with Normal Renal Arteries and No Precipitating Risk Factors

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Why the study?

Does discontinuation of RAAS blockade improve eGFR in CKD patients with late-onset azotemia and normal renal arteries?

Population

5 Caucasian CKD patients with >25% higher serum creatinine and normal MRA without precipitating factors, on…

Comparison

Discontinuation of RAAS blockade vs Baseline (prior to discontinuation)

Design

Case_series

Follow-up

29.6 (20-43) months

Authors

MOMacaulay OnuigboUniversity of Vermont NONnonyelum T.C. OnuigboUniversity of Wisconsin–Eau Claire

Discussion

Member takes

Implication

May support cautious RAAS withdrawal in select late azotemia; hypothesis-generating and should not yet change practice.

Key Points

To evaluate whether patients with chronic kidney disease on long-term RAAS blockade can develop delayed azotemia despite having normal major renal arteries and no precipitating triggers.
Followed 5 patients (1 male, 4 females; mean age 68 years) enrolled between September 2002 and February 2005 from a prospective study who experienced a >25% rise in serum creatinine after stable RAAS blockade (mean duration 34.6 months).
Excluded large-vessel renal artery stenosis using magnetic resonance angiography (MRA), discontinued RAAS blockade, and tracked estimated glomerular filtration rate (eGFR) via the MDRD formula over a median follow-up of 29.6 months (range 20–43 months).
Prior to drug discontinuation, baseline eGFR significantly declined from 28.4 ± 7.1 to 17.0 ± 7.4 ml/min/1.73 m² BSA (p < 0.001) at enrollment, requiring temporary hemodialysis in one patient.
Following the cessation of RAAS blockade, eGFR significantly improved from 17.0 ± 7.4 to 24.6 ± 9.5 ml/min/1.73 m² BSA (p = 0.009) at 29.6 months, with zero mortalities observed.

Structured PICO

Does discontinuation of RAAS blockade improve eGFR in CKD patients with late-onset azotemia and normal renal arteries?

Population

5 Caucasian CKD patients (1 male, 4 female; age 68 years) with >25% higher serum creatinine and normal MRA without precipitating factors, on stable doses of RAAS blockade for >3 months.

Intervention

Discontinuation of RAAS blockade

Comparator

Baseline (prior to discontinuation)

Outcome

eGFR by MDRDsurrogate

Discontinuation of RAAS blockade in CKD patients with late-onset azotemia and normal renal arteries may improve eGFR, suggesting microvascular arteriolar narrowing as a potential mechanism for renal decline.

Cite This Study

Onuigbo et al. (2008) studied this question.

synapsesocial.com/papers/6a7e237b203fea68b203b4e1 https://doi.org/10.1080/08860220701742161

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Late Onset Azotemia from RAAS Blockade in CKD Patients with Normal Renal Arteries and No Precipitating Risk Factors

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Late Onset Azotemia from RAAS Blockade in CKD Patients with Normal Renal Arteries and No Precipitating Risk Factors

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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