Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The formation of various types of kidney stones is strongly influenced by urinary pH. An alkaline pH favors the crystallization of calcium- and phosphate-containing stones, whereas and acidic urine pH promotes uric acid or cystine stones. The activity of many transport processes involved in calcium, citrate and phosphate handling are sensitive to changes in systemic or local pH as shown for several phosphate transporters, the citrate transporter NaDC1 and the TRPV5 calcium channel. Defects in urinary acidification (excretion of inappropriately alkaline or acidic urines, respectively) contribute to kidney stone disease. The low excretion of ammonium in patients with metabolic syndrome has been linked to more acidic urine and a higher incidence of uric acid stones. In this state, insulin resistance may reduce ammonium excretion by the proximal tubule. On the other hand, defensive mechanisms may protect from kidney stone formation in conditions such as hypercalciuria where high luminal calcium concentrations stimulate urinary acidification and reduce urinary concentration via a calcium-sensing receptor, resulting in the excretion of acidic and diluted urine. This review will discuss a few aspects that relate to the capacity of the kidney to regulate pH and its impact on the excretion of solutes that participate in the formation or prevention of stones.
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PMID:Urinary pH and stone formation. 2117 Aug 75

The association between nephrolithiasis and many chronic kidney diseases suggests a common causative link. There are indications that stone formation can lead to hypertension, diabetes, chronic disease and myocardial infarct. The reverse also appears to be true in that diabetes and hypertension can lead to stone formation. The production of reactive oxygen species (ROS) and the development of oxidative stress (OS) are common features of many renal and cardiovascular diseases including, hypertension, diabetes, metabolic syndrome and nephrolithiasis. It is my hypothesis that oxidative stress produced by one disease may lead to another under suitable conditions. For example mild hypercalciuria, hyperoxaluria, hypocitraturia which under normal conditions may just be a curiosity or nuisance can promote crystallization when cells are injured by ROS produced by the co-morbid condition. On the other hand OS produced during or as a result of nephrolithiasis may promote hypertension or diabetic nephropathy.
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PMID:Stress oxidative: nephrolithiasis and chronic kidney diseases. 2339 35

A definite epidemiological association exists between kidney stone disease and arterial hypertension, but the pathophysiological mechanisms are still not fully understood. Hypercalciuria or inflammation and oxidative stress have been proposed as possible links. However, there is more convincing evidence that the association between nephrolithiasis and hypertension may be considered as a part of the association between kidney stone disease, metabolic syndrome and atherosclerosis. From a clinical point of view, this association represents a crucial aspect of the clinical management of patients affected by kidney stone disease. In order to implement early prevention and treatment of cardiovascular and/or renal damage physicians should be encouraged to assess individual cardiovascular risk factors in any adult with kidney stones. Consequently, patients with kidney stones need a comprehensive approach rather than an intervention limited to the urinary tract and focused on stone resolution and recurrence prevention. It is time to view kidney stone disease as a systemic disorder, associated to or predictive of hypertension, chronic kidney disease, bone and cardiovascular damage. All these conditions negatively affect patient prognosis. This multi-systemic approach could increase the clinical impact of the kidney stone clinic.
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PMID:Nephrolithiasis and hypertension: possible links and clinical implications. 2457 80

In this review, we analyze the etiopathogenic principles of urinary lithiasis formation. In the kidney, calcifications that may cause renal lithiasis are produced as a consequence of processes that injury the urothelium at the papilla and Bellini's ducts. With the improvement of imaging techniques, mainly micro CT scan, it is possible to detect them and we may be able to anticipate to the formation of lithiasis. As we well know, there are different factors that influence the formation of the calculi depending on their composition. In calcium lithiasis it is key to review the modification of the categories of hypercalciuria, we currently distinguish two types instead of three, thanks to the fasting calcium/ creatinine ratio, differentiating absorptive hypercalciuria and fasting hypercalciuria. In the fasting hypercalciuria, it is important to emphasize the relationship between this factor and the loss of bone mineral density in patients with recurrent renal calcic lithiasis, so that in this kind of patients it is compulsory the study of bone metabolism by bone remodelling markers and bone densitometry. Regarding the other factors that participate in the formation of calcium lithiasis we should specially emphasize on hypercalciuria and its growing increase because of its relationship with obesity and metabolic syndrome, as well as hipocitraturia, present in an important percentage of patients and related in some cases with metabolic acidosis and osteopenia-osteoporosis too. In relation to uric acid lithiasis it should be highlighted that urinary pH is the most determinant factor and, therefore, its control and modifications would be paramount for prevention of this type of lithiasis. In the infectious lithiasis, the presence of germs that split urea is mandatory. They generate ammonia ions with the ability to injure the urothelium and to form magnesium ammonium phosphate lithiasis mainly. Regarding cystine lithiasis, rare, it was classically divided in three types and now passed to be classified in type A and B depending on the muted gene, and it is more useful to perform direct 24-hour urine measurement than screening tests which have low sensitivity. In general, we tried to give a comprehensive view of the various types of lithiasis emphasizing the most interesting clinical points for the urologist.
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PMID:[Etiopathogenic factors of the different types of urinary litiasis.] 2822 Nov 41