RENAL TUBULAR ACIDOSIS OF PYELONEPHRITIS WITH RENAL STONE DISEASE

Renal acidifying power was tested in about 600 patients with renal stone disease, the short ammonium chloride loading test of Davies and Wrong (1957) being used. Twenty-four patients were unable to acidify their urine to pH 5.4 (group A); all of them had evidence of chronic pyelonephritis. These patients are compared with 24 stone patients with pyelonephritis and normal acidifying power (group B). The group A patients tended to have a longer history of pyelonephritis than the group B patients and were more liable to bilateral stone formation. Their excretion of titratable acid tended to be lower and their excretion of ammonium higher than in group B. Concentrating power tended to be more impaired in group A than in group B cases, but was low relative to creatinine clearance in both groups. Only five group A cases and no group B cases were actually acidotic at the time of observation and electrolytes were essentially normal in both groups. Serum calcium and phosphorus were normal in both groups, except in two cases of osteomalacia in group A, but the serum Ca x P products tended to be low. Serum alkaline phosphatase was raised in those two cases and in one case with Paget's disease. Phosphate excretion tended to be high relative to serum phosphate in group A. Calcium output per 24 hours was related to creatinine clearance in both groups but tended to be lower in group A than in group B. Calcium excretion per 100 ml. of glomerular filtrate tended to be raised in both groups. Urinary citrate tended to be low in group A. It is concluded that a form of acidifying defect indistinguishable from that in congenital renal tubular acidosis, but generally not accompanied by overt acidosis, can be acquired from pyelonephritis associated with stone disease. Postoperative long-term chemotherapy in a few cases has so far prevented stone recurrence. © 1968, British Medical Journal Publishing Group. All rights reserved.