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Renal acidification in sickle-cell disease

J R Oster, L E Lespier, S M Lee

The Journal of Laboratory and Clinical Medicine

|September 1, 1976

Summary

Patients with sickle-cell disease (HbSS) show impaired renal acidification, with some exhibiting incomplete distal renal tubular acidosis. This study evaluated their kidney function and acid-base balance compared to controls.

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Area of Science:

Nephrology
Hematology
Acid-Base Physiology

Background:

Sickle-cell disease (HbSS) is associated with various organ complications, including potential renal abnormalities.
Renal acidification is crucial for maintaining acid-base homeostasis.

Purpose of the Study:

To evaluate renal acidification in patients with sickle-cell disease (HbSS).
To compare renal acidification responses to acid and bicarbonate loading in HbSS, sickle-cell trait (HbAS), and control subjects.
To investigate potential links between renal acidification defects and other renal functions in HbSS.

Main Methods:

Oral ammonium chloride (NH4CI) and sodium bicarbonate (NaHCO3) loading tests were administered.
Urine pH, blood pH, pCO2, and bicarbonate levels were measured.
Renal function tests including PAH clearance, inulin clearance, and maximal concentrating ability were assessed.

Main Results:

Six of 20 HbSS subjects demonstrated an abnormal minimal urine pH (>5.3) after NH4CI loading, suggesting incomplete distal renal tubular acidosis.
The HbSS group showed a higher mean urine pH compared to controls and HbAS subjects.
Maximal concentrating ability was reduced in both HbSS and HbAS groups, more significantly in HbSS.
PAH and inulin clearance were higher in HbSS subjects.

Conclusions:

A subset of patients with sickle-cell disease exhibit incomplete distal renal tubular acidosis.
Renal acidification abnormalities in HbSS may coexist with altered renal hemodynamics and concentrating ability.
The underlying mechanism for the observed renal acidification defect in HbSS remains undetermined.

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