Kidney number, abnormal

Allyl chloride was fetotoxic to rats exposed during gestation to 300ppm, which also caused considerable maternal toxicity in the form of kidney and liver injury. It was a testicular toxicant in mice, causing decreased testes weight, reduced numbers of spermatids, and increased frequency of abnormal sperm after a single subcutaneous injection to male mice at one-fifth the LDso. ... 

Vitamin D deficiency remains the most common cause of rickets and osteomalacia in the world, with the exception of the United States and the Scandinavian countries where most dairy products are supplemented with this vitamin. This deficiency can be caused either by dietary habits or by insufficient exposure to ultraviolet light. The same type of symptoms can be observed when there is interruption of the normal vitamin D metabolic pathways due to a number of liver and/or kidney diseases. In addition, a number of inherited factors can lead to different types of vitamin D resistance which require massive supplements of vitamin D and/or minerals. Extensive reviews have been published depicting both the clinical features and their most likely causes, as well as the possible treatments of the different types of clinical disorders resulting from vitamin D deficiencies [113-117], The newly defined role for l,25(OH)2D3 upon the hematopoietic system could also have clinical relevance in bone disorders such as osteoporosis where patients have been shown to possess abnormal T-cell subsets [118]. 

In light of the increased number of man-6-P/IGF-II receptors in I-cell fibroblasts, the above interactions of IGF could have far-reaching effects. For example, I-cell disease has not been typically associated with abnormalities in phos-phorous/calcium metabolism. The extensive skeletal deformities could involve impairment of mechanisms of orderly calcium deposition. Rather than resulting from a primary disorder of calcium metabolism, it is possible that the bone lesions in I-cell disease are secondary to altered lysosomal processing events in the kidney or liver. 

Fig. 4. Number of patients examined, divided according to the urological disease and number of those showing abnormal levels of tryptophan metabolites spontaneously excreted. Percentage of the abnormally excreting patients is given A = bladder tumors B = extrabladder tumors C = kidney tumors D = urological diseases (non-neoplastic).

Supportive care must be instituted for patients accidentally exposed to aerosol contents via topical, inhalation, or oral routes. A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure. 

Embryonic exposure to vinclozolin, an antiandrogenic endocrine disruptor, has been shown to promote prostate disease, kidney disease, immune system abnormalities, testicular abnormalities, breast and other tumor development, and a number of blood abnormalities in the F1-F4 generations of laboratory animals. I8,91 The effects observed were noted in the adults of the four ensuing generations that followed the exposure. 

There have been reports in the literature of hypouricemia coincident with specific inborn metabolic errors, but many of these cases are attributable to defects in the kidney leading to failure of renal tubular reabsorption. It was mentioned above that the excretion of uric acid by the Dalmatian coach hound can be attributed to such a mechanism (Fll). Similarly, the hypouricemia found in the Fanconi syndrome (L4) and Wilson s disease (B12) can be attributed to kidney malfunction. These are not true examples of underproduction of oxypurines, including uric acid, since the daily output of uric acid is normal. The large number of healthy people who have extremely low serum urate values, however, may indicate that there are individuals who underproduce oxypurines but suffer no ill effects because of this. The one well-documented inborn error that results in underproduction of uric acid is xanthinuria. It has been reported in relatively few cases, probably because individuals with this metabolic abnormality who suffer no ill effects would not come to the attention of a physician. 

It is now well established that patients with Wilson s disease have grossly abnormal amounts of copper in the liver, brain, kidney, and cornea (B19, C16, U6). The copper content of other tissues may increase, but much less than in these four organs that are the site of the pathological changes in this disease. Increased urinary copper excretion is also characteristic of the disease as evidence for this a large number of references to pertinent literature can be found in Cumings monograph (C16). 

Extracorporeal medical machines (e.g., artificial kidney, pump-oxygenator) perfused with blood have been an effective part of the therapeutic armamentarium for many years. These devices all rely on systemic heparinization to provide blood compatibility. Despite continuous efforts to improve anticoagulation techniques, many patients still develop coagulation abnormalities with the use of these devices (1-3). Even longer perfusion times may occur with machines such as the membrane oxygenator. In such cases, the drawbacks of systemic heparinization are multiplied (4). A number of ap-... 

A patient with chronic kidney disease (CKD) is defined as having a decreased renal function of 60%, persisting abnormal urine analysis for three months or longer, or a number of (or persisting) renal morphological abnormalities. 

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