Renal stones types

More than 30 different types of renal stones have already been identified (S4). The most common types are illustrated in Table 1. Because most renal stones consist of calcium-containing concrements, and especially oxalate (72.4%) (S4), the primary focus of this discussion will be on the formation of calcium oxalate-containing stones. 

Renal stones (calculi) produce severe pain and discomfort, and are common causes of obstruction in the urinary tract (Fig. 2). Chemical analysis of renal stones is important in the investigation of why they have formed. Types of stone include ... 

Although most of this discussion concerns stones originating in the kidney, lithiasis may be primary to the bladder or the ureters. Whereas phosphate and oxalate stones develop more frequently in the kidney, bladder stones are usually of the urate type. The geographical distribution of urinary lithiasis varies considerably. The disease is common in central Russia, China, Canton, and India. However, in India and China bladder stones are the type seen most often, whereas renal stones are more common in America. 

Further genes involved in other conditions responsible for renal stone development among many others could be identified e.g. osteopetrosis with tubular acidosis type 1 (xanthinoxidase), hyperoxaluria typel (alanine-glyoxylate-aminotrans-ferase), adenine-phosphoribosyltransferase deficiency (ATRTase), distal tubular acidosis and primary hypomagnesemia. 

The future of phosphate fibers should be very bright when the patents on the composition expire in 1999. In the author s mind there has never been a safety issue with phosphate fibers or any other inorganic phosphate that does not contain a toxic cationic or anionic function. Phosphates such as sodium, potassium, calcium, magnesium, ammonium, and hydrogen have never caused a problem of any type with perhaps the exception of renal stones. In this case it may be more of a condition than the cause of a condition. Urine is known to be saturated with respect to calcium phosphates. Some threshold agent or other mechanism that is poorly understood keeps kidneys from becoming completely calcified even in the healthiest of persons. 

Strain on the efficacy of a particular technique. The main obstacle for diagnosing them is very subtle visual difference between their sonograms. One possible approach can be texture analysis, because as the composition of the renal stone changes, it produces changes in acoustical properties of the tissue, which could be detected by ultrasound as a textural pattern different for each type. For example, ultra sono graphic images of different concentrations of calcium oxalate monohydrate, dihydrate and carbonate apatite are very similar and it is very difficult, even for an experienced clinician, to perform the diagnosis about the existence and type. Therefore, a reliable non-invasive method for early detection and differentiation of these different is clearly desirable, (see Fig. 1). 

Uric acid excretion is reduced in patients with chronic kidney disease, putting them at risk for hyperuricemia. In patients with persistently acidic urine and hyperuricemia, uric acid nephrolithiasis can occur in up to 25% of patients in severe cases, uric acid stones can cause nephropathy and renal failure. Extreme hyperuricemia can occur because of rapid tumor cell destruction in patients undergoing chemotherapy for certain types of cancer (see Chap. 85). 

An association between the use of 5-ASA in patients with chronic inflammatory bowel disease and the development of a particular type of chronic tubulo-in-terstitial nephritis is difficult to interpret since renal involvement in chronic inflammatory bowel disease may be an extra-intestinal manifestation of the underlying disease [110]. Extra-intestinal manifestations of chronic inflammatory bowel disease are well recognized. The most frequent renal complications are oxalate stones and their consequences such as pyelonephritis, hydronephrosis and on the long-term amyloidosis [111, 112]. As for many drugs, reversible acute interstitial nephritis has been described [90]. 

There is epidemiologic evidence to suggest an increased prevalence of duodenal ulcers in patients with certain chronic diseases, but the pathophysiologic mechanisms of these associations are uncertain. A strong association exists in patients with systemic mastocytosis, multiple endocrine neoplasia type 1, chronic pulmonary diseases, chronic renal failure, kidney stones, hepatic cirrhosis, and ai-antitrypsin deficiency. An association may exist in patients with cystic fibrosis, chronic pancreatitis, Crohn s disease, coronary artery disease, polycythemia vera, and hyperparathyroidism. 

Renal disease is a eommon complication of hyperuricaemia. Several types of renal disease have been identified. The most comnutn is urate nephropathy which is caused by the deposition of urate crystals in renal tissue or the urinary tract to form urate stones. This mtiy be associated with chronic hyperuricaemia. Acute renal failure can be cau.sed by the rapid precipitation of uric acid crystals w hich commonly occurs during treatment of patients with leukaemias and lymphomas. In the acute tumour lysis syndrome (p. 129), nucleic acids are released as a result of tumour cell breakdown and arc rapidly metabolized to uric acid. 

Oxalate, produced from glycine or obtained from the diet, forms precipitates with calcium. Kidney stones (renal calculi) are often composed of calcium oxalate. A lack of the transaminase that can convert glyoxylate to glycine (see Fig 39.6) leads to the disease primary oxaluria type I (PH 1). This disease has a consequence of renal failure attributable to excessive accumulation of oxalate in the kidney. 

Glycine Glycine transaminase Glyoxylate Primary oxaluria type 1 Renal failure due to stone formation... 

In its role in purine catabolism, XnDH catalyzes sequential hydroxylation of the C-2 and C-8 atoms of hypoxanthine, converting it first to xanthine and then to uric acid (eqn (7.1), keto forms shown). In humans, enzyme deficiency is associated with xanthinuria types I and II, the symptoms of which include urinary tract infections, myopathy, arthritis, arthralgia, kidney stones and acute renal failure, while over-activity causes hyperuricemia and the deposition of urate salts in the joints leading to gout. ... 

The frequency of hyperuricosuria, according to our definition, and renal acidification defects (RTA) are presented in Table 2. Ten patients who had both hyperuricosuria and RTA had the incomplete form of the defect. Eight had the proximal form and the other 2 the distal form. In the normouricosuric group 7 had the proximal type and 3 the distal type, all of the incomplete form. The duration of the stone disease was the same in both groups. Hyperuricosuric patients had a high operation rate. But when consideration was taken of acidification deflects, only hyperuricosuric patients with RTA exhibited the higher operation rate (Fig. 1). 

The urine pH is important for the development of stones. Calcium stones develop preferentially at an alkaline pH and uric acid stones at acid pH. Among other factors that modulate renal pH, infection is critical. For example, Proteus species split urea to yield ammonia therefore, infection by this type of bacteria is often followed by stone formation. 

Carbonic anhydrase inhibitors are used in the treatment of glaucoma and, less commonly, in the treatment of certain types of stones in the renal tract. 

There are sixteen to twenty-four cases of nephrolithiasis per 10,000 persons reported in the United States yearly. Males have a three-fold to four-fold increased risk of the development of renal calculi over females. Uric acid and calcium stones are the most prevalent types of calculi found in men, whereas infectious stones are more common in females. 

Nephrolithiasis and/or nephrocalcinosis may be additional findings on sonography and can be confirmed on plain abdominal radiograph. Renal or urinary tract stones are found in uropathies caused by recurrent urinary infections and urine stasis. Nephrocalcinosis may be the consequence of acid-base disturbance and hypercalciuria in congenital tubulopathies. The presence of nephrocalcinosis and nephrolithiasis favors primary hyperoxaluria type 1 (PH 1) as diagnosis. This autosomal recessive inherited disease is caused by a deficiency of the liver-specific peroxisomal enzyme alanine-gly-... 

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