Crystal nephropathy

Tubule obstruction. Given certain physicochemical conditions, crystals can deposit within the tubular lumen. Methotrexate, for example, is relatively insoluble at low pH and can precipitate in the distal nephron when the urine is acid. Similarly the uric acid produced by the metabolism of nucleic acids released during rapid tumour cell lysis can cause a fatal urate nephropathy. This was a particular problem with the introduction of chemotherapy for leukaemias until the introduction of allopurinol it is now routinely given before the start of chemotherapy to block xanthine oxidase so that the much more soluble uric acid precursor, hypoxanthine, is excreted instead. Crystal-nephropathy is also a... 

A renal biopsy demonstrated crystal nephropathy in a cryostat section under polarised light. There was much tubular atrophy with extensive tubular epithelial giant cell transformation in the cortex and medulla. All crystals dissolved on fixing in formalin. 

The value of ultrasonography in identifying crystal nephropathy when the diagnosis is obscured by renal failure has been demonstrated in both cases. This is especially relevant when renal function is so... 

This study has shown that deposition of crystals in the renal tubules even for short periods, can produce irreversible damage, not only locally, but also affecting other parts of the nephron. It is hoped that this experiment, together with a long term study now underway, will provide a model for crystal nephropathy in man. 

The combination of guanine and allopurinol produced an acute crystal nephropathy in the pig and permanent renal damage ( ). 

Diuretics Loops, thiazides, triamterene Acute interstitial nephritis, crystal nephropathy... 

The answer is c. (Hardman, pp 649—650.) Acute hyperuricemia, which often occurs in patients who are treated with cytotoxic drugs for neoplasic disorders, can lead to the deposition of urate crystals in the kidneys and their collecting ducts. This can produce partial or complete obstruction of the collecting ducts, renal pelvis, or ureter. Allopurinol and its primary metabolite, alloxanthine, are inhibitors of xanthine oxidase, an enzyme that catalyzes the oxidation of hypo xanthine and xanthine to uric acid. The use of allopurinol in patients at risk can markedly reduce the likelihood that they will develop acute uric acid nephropathy. 

In acute uric acid nephropathy, acute renal failure occurs as a result of blockage of urine flow secondary to massive precipitation of uric acid crystals in the collecting ducts and ureters. This syndrome is a well-recognized complication in patients with myeloproliferative or lymphopro-liferative disorders and results from massive malignant cell turnover, particularly after initiation of chemotherapy. Chronic urate nephropathy is caused by the long-term deposition of urate crystals in the renal parenchyma. 

Pharmaceutical therapy of acute arthritis of crystal-deposition disease is effective, in particular for gout and hyperuricemia. Treatment is directed towards termination of acute arthritis, prevention of recurring attacks and prophylaxis and reversal of complications of chronic gout. Such complications include tophi, urolithiasis, nephropathy and with hyperuricemia associated medical problems that can be prevented, inhibited, and sometimes reversed. 

Nephrotoxicity Pre-renal failure, e.g. hypotension following 3 lactam-induced anaphylaxis Obstructive nephropathy, e.g. crystal deposition following cephalosixrin administration... 

Martinez E, Mommeja-Marin FI, Estepa-Maurice L, Beaufils FI, Boche, M, Daudon M, Deray G, and Katlama C. 1998. Indinavir crystal deposits associated with tubulointerstitial nephropathy. Nephrol Dial Transplant 13 750-753. 

Viscosity of THP solutions increases markedly when the sodium chloride concentration is > 60 mM. Increasing the concentration of calcium and/.or a reduction in pH also increase viscosity and may account for the involvement of THP in the pathogenesis of cast nephropathy and tubulointerstitial nephritis. THP appears to have an inhibitory effect on urinary crystal arrgegation [154] and may play a role in preventing renal stone formation [155]. In some humans with calcium oxalate nephrolithiasis, a molecular abnormality of THP has been detected [156]. Other studies showed decreased urinary levels of THP in patients with nephrolithiasis [157, 158]. A relative deficiency in THP has been associated with impaired inhibition of crystal adhesion to renal epithelial cells instone formers [159]. 

Colebunders R, Depraetere K, De Droogh E, Kamper A, Corthout B, Bottiau E. Obstructive nephropathy due to sulfa crystals in two HIV seropositive patients treated with sulfadiazine. Jbr-Btr. 1999 Aug 82(4) 153-4. 

In an in vivo animal study, at doses not causing crystalluria or tissue crystal deposition, short term exposure to acyclovir caused increased renal vasoconstriction and an associated fall in renal blood flow and single nephron plasma flow [22]. Longer-term treatment resulted in a fall in glomerular ultrafiltration coefficient. Thus, it is not clear whether the pathogenesis of acyclovir-induced AKI in humans reflects an obstructive nephropathy from intratubular precipitation of acyclovir, a hemodynamic response, or a type of toxic, immunologic, or hypersensitivity reaction. It is also possible that more than one process may be involved. 

In 2003, Desmeules et al. described a new pattern of renal failure resulting from the use of OSPS [29]. A 71-year-old female with a baseline creatinine of 1.0 mg/ dl presented with acute kidney injury and a creatinine of 4.5 mg/ dl two weeks following the use of OSPS. Renal biopsy revealed numerous tubular calcium phosphate deposits. Scanning electron microscopy and energy-dispersive x-ray microanalysis revealed that the calcium phosphate deposits formed crystals of hydroxyapatite. The patient s creatinine declined to 1.7 mg/dl at one year of follow-up. The authors described the process as "phosphosoda-induced nephrocalcinosis" and proposed the term "acute phosphate nephropathy". 

Obstructive nephropathy is the result of mechanical obstruction to urine flow following glomerular filtration. This may be due to intratubular obstruction from crystal precipitation within the tubules of the kidney or extrarenal obstruction of the ureters or bladder. Pain, hematuria, and infection may precede a significant rise in serum creatinine. 

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. 

B. Vitamin C. Chronic excessive use and large intravenous doses can produce increased levels of the metabolite oxalic acid. Urinaiy acidification promotes calcium oxalate crystal fomiation, which can result in nephropathy or acute renal failure. 

B. Vitamin C. Calcium oxalate crystals may cause acute renal failure or chronic nephropathy. 

In summary these children had features in common which made it difficult to identify the underlying enzyme abnormality and its relationship to their presentation in renal failure. Both had raised plasma uric acids not unusual in severe renal failure but in these children the magnitude was the important factor The crystals or stones causing the nephropathy could both have been identified as uric acid Urinary uric acid on a creatinine basis was not raised in either The severe renal damage at such an early age in both underlines the importance of early and correct identification of these defects, especially APRT deficiency, which can be treated successfully with allopurinol and such severe renal damage need never occur. ... 

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