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Nephrol Dial Transplant (1999) 14: 2556-2558
© 1999 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

What is new in primary hyperoxaluria?

Ernst Leumann1 and Bernd Hoppe2

1 Nephrology Unit, University Children's Hospital, Zurich, Switzerland and 2 Nephrology Unit, University Children's Hospital, Cologne, Germany

Correspondence and offprint requests to: Prof. Ernst Leumann, University Children's Hospital, Steinwiesstrasse 75, CH-8032 Zurich, Switzerland.

Introduction

Although the majority of renal stones both in children and in adults are formed by calcium oxalate (CaOx), few patients actually suffer from a primary metabolic defect leading to excessive endogenous production of oxalate. Nevertheless, there is considerable interest in primary hyperoxaluria (PH)—the prototype and model of hyperoxaluria—since a better understanding of the pathogenic mechanisms is also expected to help the much larger group of patients with urolithiasis not suffering from PH. Two recent symposia (NIH Workshop, 8–9 December 1998, Bethesda, USA and 5th Workshop on PH, 12–13 March 1999, Zurich, Switzerland) have dealt with these problems [1]. It has become obvious that PH is a highly complex disorder, consisting of two well-described forms (PH1 and PH2) and of further conditions.

Toxicity

Oxalate is a useless end-product of metabolism and is normally completely excreted by the kidneys (normal excretion <0.5 mmol (45 mg)/24 . . . [Full Text of this Article]

Intestinal absorption

Plasma oxalate and CaOx saturation

Liver biopsy

Primary hyperoxalurias

PH1
Therapy of PH1
Transplantation
Prospects of gene therapy
PH2
Atypical PH

Conclusion

Notes

References


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