Hyperglobulinemic Renal Tubular Acidosis

Report of Two Cases

  1. DONNA K. MCCURDY, M.D.;
  2. GIBBONS G. CORNWELL III, M.D.; and
  3. VICTOR J. DEPRATTI, M.D.
  1. Requests for reprints should be addressed to Donna K. McCurdy, M.D., 860 Gates Bldg., Hospital of the University of Pennsylvania,
    Philadelphia, Pa. 19104
    .

Excerpt

Renal tubular acidosis is a syndrome in which a specific inability of the renal tubule to lower urine pH normally is associated with renal bicarbonate wastage and, ultimately, hyperchloremic acidosis. Other common but by no means invariable manifestations of the syndrome include hypokalemia due to renal potassium wastage, nephrolithiasis and nephrocalcinosis, a vasopressin-resistant nephrogenic diabetes insipidus, hypercalciuria, decreased citrate excretion, and osteomalacia (1-4). Although the primary form of this syndrome occurs both familially and sporadically, unassociated with other diseases, secondary renal tubular acidosis may develop in the course of a number of disease states that in various ways may lead

This 100-word excerpt has been provided in the absence of an abstract.

Acknowledgments

The authors wish to thank Drs. Howard M. Rawnsley and Dean A. Arvan for analysis of serum protein fractions, Dr. Burton Zweiman for determination of antinuclear factor, and Dr. Arnold J. Rawson for fluorescent anti-gamma-globulin studies of the renal biopsy specimen. We also wish to thank Miss Cordelia Schute and the staff of the Clinical Research Center and Miss Elizabeth Cameron for their assistance in studying and caring for both patients, and Lidia Kosolapovs, Leonids Kosolapovs, Katherine Wishnevski, Carmen D'Angelo, Helaine Kandel, Marlene Weiner, and Heddy Bowman for technical assistance. Finally, we wish to thank Dr. Martin Goldberg both for helpful criticism of the manuscript and for his support, and Dr. David Devon for allowing us to study his patient (N. M.).

Article and Author Information

  • From the Renal-Electrolyte and Hematology Sections, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pa.

  • This work was supported by grants 5 R01 HE00340-18, 5R01 HE-07284-04, 05, and 5M01, FR 40-07, the U. S. Public Health Service, Washington, D. C.

  • Drs. Cornwell and DePratti were Trainees in Hematology supported by training grant TI AM 5228, the U. S. Public Health Service.

    • Received April 28, 1967.
    • Accepted May 1, 1967.
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