Titlebook: Calculus Disease; Graeme R. D. Catto (Reader in Medicine, Harkness F Book 1988 Kluwer Academic Publishers 1988 Calc.Volume.boundary elemen

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M. Passatore,C. Grassi,F. Deriuf knowledge, a minority of stone formers can be reassured that all the causative factors have been identified, and that, by taking known appropriate action, the patient can be virtually guaranteed a cure with a minimal chance of further stone formation. This applies in primary hyperparathyroidism, i

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M. Passatore,C. Grassi,F. Deriuhallmark of cystinuria. Transport systems in the small intestine are also affected, leading to malabsorption of these amino acids (Figure 4.1). The biochemical defects will be referred to but have been reviewed extensively elsewhere.. The disorder, which is inherited in an autosomal recessive patter

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Rebecca Craik,Richard Herman,F. Ray Finley stone formation. The initial section of this chapter deals with the presentation, investigation and treatment of hypercaccaemic states in general. Subsequently, specific hypercalcaemcc disorders are discussed, with particular emphasis on those associated with renal stone disease (Table 1.1).

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M. Passatore,C. Grassi,F. Deriu, the urinary calcium was brought into the normal range, yet over one half continued to develop new or larger calculi. It follows that there must be other unidentified factors which are in part responsible for the continued urolithiasis, and a possible explanation for this is discussed at the end of this chapter.