ISSN:1660-8151    

DOI:10.1159/000180429

出版商:S. Karger AG    

年代:1975

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000180430

出版商:S. Karger AG    

年代:1975

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000180431

出版商:S. Karger AG    

年代:1975

数据来源: Karger

摘要:

The origin of uric acid, metabolic pathways of purine metabolism and the disposition of uric acid in normal man are reviewed. Two thirds of the uric acid is normally excreted through the kidney while one third gains entrance to the gut where it undergoes uricolysis. The pathogenesis of hyperuricemia in primary and secondary gout is discussed. Increased production or decreased excretion of uric acid are the two principal mechanisms of hyperuricemia. The known biochemical defects associated with primary overproduction gout are outlined. Extrarenal uricolysis assumes a greater role when the renal excretion of uric acid is compromised.

ISSN:1660-8151    

DOI:10.1159/000180432

出版商:S. Karger AG    

年代:1975

数据来源: Karger

摘要:

The development of our knowledge of the intrarenal processes involved in the control of urate excretion in normal man is summarized. Although there are many gaps in our current knowledge, and different interpretations may be given to the available data, current evidence seems to favor the existence of extensive tubular reabsorption of urate following its glomerular filtration. Subsequently, tubular secretion of urate and the reabsorption of an unknown amount of the secreted urate probably take place. For reasons discussed, it seems most likely that the regulation and control of urate excretion are accomplished through modulations in tubular secretion, post-secretory reabsorption, or both.

ISSN:1660-8151    

DOI:10.1159/000180433

出版商:S. Karger AG    

年代:1975

数据来源: Karger

摘要:

Several aspects of the comparative physiology and pharmacology of renal urate handling are considered; with special attention to bidirectional transport, the existence of intrarenal urate synthesis and degradation in certain species, and the nature and sites of the reabsorptive and secretory processes. Interspecies variations in the sensitivity of the kidney to uricosuric agents and the degree of specificity of the secretory mechanism are discussed. A variety of techniques, especially as applied in certain nonhuman primates, have led to a concept of very rapid trans-tubular fluxes of urate – a concept which may apply in ma

ISSN:1660-8151    

DOI:10.1159/000180434

出版商:S. Karger AG    

年代:1975

数据来源: Karger

摘要:

The uricosuric properties of acetazolamide were investigated in order to elucidate the relationship between changes in proximal tubular sodium reabsorption and urate excretion in man. Acetazolamide produced a modest uricosuric response which was not suppressible by pyrazinamide. Alkalinization of the urine with sodium bicarbonate elicited an even smaller increment in the urate clearance. If urinary alkalinization does play a role in the uricosuric response to acetazolamide, it probably decreases urate reabsorption within the distal nephron. The present studies, when taken together with previous work, suggest that alterations in proximal tubular sodium and water reabsorption probably do not play an important role in the normal control of urate excretion or in the pathogenesis of hyperuricemic states. Diuretic-induced hyperuricemia occurring during extracellular fluid volume depletion probably results from either diminished tubular secretion of urate, accelerated postsecretory urate reabsorption, or both.

ISSN:1660-8151    

DOI:10.1159/000180435

出版商:S. Karger AG    

年代:1975

数据来源: Karger

摘要:

Abnormalities of renal handling of urate occur in a wide variety of physiological and pathological conditions and are mediated by factors including renal blood flow, glomerular filtration rate, urine flow rate, urinary constituents, metabolites, hormones and drugs. The determination of the aetiological factors in each abnormal situation is complex and the problem is discussed in relation to a variety of conditions including renal tubular disorders and metal intoxications, hypertension, toxaemia of pregnancy, glycogen storage disease, fructose administration, hereditary fructose intolerance, as well as obesity, regular alcohol consumption and hyperlipoproteinaemia. Apart from those diseases, usually genetically determined, which are associated with excessive production of urate, the most common causes of hyperuricaemia act at a renal level and result in a reduction in the net renal excretion of urate.

ISSN:1660-8151    

DOI:10.1159/000180436

出版商:S. Karger AG    

年代:1975

数据来源: Karger

摘要:

Since approximately two thirds of daily urate production is normally excreted by the kidney, intrinsic renal disease resulting in abnormalities of urate excretion may have a profound effect upon urate homeostasis. Alterations in the pattern of urate excretion encountered in chronic renal failure are reviewed in depth, with a description of adaptive mechanisms for urate excretion which develop in residual nephrons, as exemplified by the remaining normal kidney of transplant donors. In addition, abnormalities in urate excretion in the presence of a normal complement of nephrons are described. Diminished urate excretion per nephron appears to be responsible for hyperuricemia in some patients with gout, while a variety of tubular defects resulting in excessive renal urate excretion have been documented as the basis for some cases of hypouricemia.

ISSN:1660-8151    

DOI:10.1159/000180437

出版商:S. Karger AG    

年代:1975

数据来源: Karger

摘要:

The three general types of renal pathology associated with hyperuricemia are reviewed. Factors influencing urate solubility are discussed, as well as the effect of uricosuric drugs on renal urate handling, with particular emphasis upon their efficacy in competing with urate for protein binding sites. In addition, a new experimental model of hyperuricemic nephropathy is described which could yield valuable data concerning the complex relationships between hyperuricemia, urate deposition and renal function.

ISSN:1660-8151    

DOI:10.1159/000180438

出版商:S. Karger AG    

年代:1975

数据来源: Karger