Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study the mechanism of dystrophic calcification, an anoxic incubation of rat renal cortex in a tissue culture medium was performed in vitro. Calcium and phosphate in the medium were adjusted to 1.6 and 1.2 mM/1 respectively. Calcification occurred in apposition to the inner surface of membranous cellular degradation products and associated with the flocculent densities within the degenerate organelles. The chemical nature of the flocculent density was not determined. In view of the known affinity of calcium for acidic phospholipids, particularly phosphatidyl serine (PS), which lines the inner surface of the plasma membrane, calcification along the inner surface of membrane was thought to be related to the presence of PS. Accumulation of calcium in mitochondria, which is presumably dependent upon residual substrate for energy production, appeared to cause calcification as well. Amorphous calcium phosphate in the form of spheroids, and possibly fine fibrils and granules, also appeared to play a role in calcification by their transformation into apatite. The seemingly simple phenomenon of tissue calcification is complex. Nephrocalcinosis in vitro is remarkably similar to the calcification in acute tubular necrosis in vivo, and is a convenient model with which to study the mechanism of calcification. It is concluded that the cellular degradation products are the initial loci of calcification and have a likely role in urolithiasis.
 ...
PMID:Nephrocalcinosis in vitro. 664 38

A 9-year-old castrated male domestic shorthair cat with dysuria, anorexia, vomiting, and lethargy was admitted to the veterinary teaching hospital. A large, firm mass was palpable in the ventral cervical region. Hypercalcemia, azotemia, and nonregenerative anemia were evident on serum biochemical analysis and CBC, and multiple uroliths were detected by abdominal radiography. At necropsy, light microscopy of the ventral cervical mass revealed a parathyroid adenocarcinoma. Light microscopy of sections of the kidneys revealed multifocal, chronic, lymphocytic/plasmacytic, tubulointerstitial nephritis, as well as moderate multifocal acute tubular necrosis. On quantitative analysis, the uroliths were composed of calcium oxalate. Determination of serum calcium concentration is indicated in cats with calcium oxalate urolithiasis to aid in detection of primary hyperparathyroidism.
 ...
PMID:Calcium oxalate urolithiasis in a cat with a functional parathyroid adenocarcinoma. 775 34

Acute renal insufficiency (ARI) complicated the course of the underlying process, including primary and secondary glomerulonephritis, interstitial nephritis, pyelonephritis, dysmetabolic nephropathies, urolithiasis, tubulopathies, renal congenitae defects and injuries in 136 of 1695 children with nephrological diseases hospitalized at Republican Pediatric Renal Center during the last decade. In 69.1% cases ARI developed by the renal type, in 23.5% cases was caused by prerenal factors, and rarely (in 7.4% cases) by postrenal factors. Renal ARI in children was caused by 5 causes, including glomerulonephritis (47%), acute tubular necrosis (19%), interstitial nephritis (14%), vascular disorders (11%) resultant from vasculitis, renal vein thrombosis, and acute crystalluria (9%) which developed in the presence of grave dysmetabolic nephropathy. Among three clinical variants of ARI the most severe was observed in renal ARI leading to grave endogenous intoxication and pronounced decompensation of renal function. More benign course of renal ARI caused by acute tubular necrosis or acute crystalluria differed significantly from prerenal ARI by a more pronounced endogenous intoxication, increased fractionated sodium excretion, and renal insufficiency index higher than 1.
 ...
PMID:[Diagnosis of acute renal failure in pediatric nephrology]. 1133 30

Renal hypouricemia is a clinical disorder attributed to an increased renal urate excretion rate and is well known to involve a high risk of urolithiasis and exercise-induced acute kidney injury (AKI). This report concerns two interesting cases of nephrotic syndrome (NS)-induced AKI associated with renal hypouricemia. A 64-year-old female (Case 1) and a 37-year-old male (Case 2) were hospitalized because of AKI (serum creatinine: 2.07 mg/dl and 3.3 mg/dl, respectively), oliguria and NS. They were treated with prednisolone and temporary hemodialysis. Renal function improved, but hypouricemia persisted during hospitalization. Histological findings in both cases led to a diagnosis of minimal change nephrotic syndrome and identification of the diuretic phase of tubulointerstitial damage because of findings such as acute tubular necrosis. Furthermore, distal tubules of Case 2 showed an amorphous mass, possibly a uric acid crystal. Analysis of the two cases with the URAT1 gene, encoded by SLC22A12, found a homozygous mutation in exon 4 (W258stop) of each one. Our cases show that patients with renal hypouricemia may be susceptible to AKI without involvement of exercise if they possess some facilitators. Renal hypouricemic patients should therefore be carefully examined for all complications from renal hypouricemia because of high risk of AKI.
 ...
PMID:Two cases of nephrotic syndrome (NS)-induced acute kidney injury (AKI) associated with renal hypouricemia. 2172 10

Renal scintigraphy is a powerful imaging method that provides both functional and anatomic information, which is particularly useful in the acute care setting. In our institution, for the past 2 decades, we have used a 25-minute renal diuretic protocol, technetium-99m ((99m)Tc) mercaptoacetyltriglycine with simultaneous intravenous injection of furosemide, for all ages and indications, including both native and transplant kidneys. As such, this protocol has been widely used in the workup of acutely ill patients. In this setting, there are common clinical entities which affect patients with native and transplant kidneys. In adult patients with native kidneys one of the most frequent reasons for emergency room visits is renal colic due to urolithiasis. Although unenhanced computed tomography is useful to assess the anatomy in cases of renal colic, it does not provide functional information. Time zero furosemide renal scintigraphy can do both and we have shown that it can effectively stratify patients with renal colic. To this end, 4 characteristic patterns of scintirenography have been identified, standardized, and consistently applied: no obstruction, partial obstruction (mild vs high grade), complete obstruction, and stunned (postdecompressed) kidney. With the extensive use of this protocol over the past 2 decades, a pattern of "regional parenchymal dysfunction" indicative of acute pyelonephritis has also been delineated. This information has proved to be useful for patients presenting with urinary tract infection and suspected pyelonephritis, as well as for patients who were referred for workup of renal colic but were found to have acute pyelonephritis instead. In instances of abdominal trauma, renal scintigraphy is uniquely suited to identify urine leaks. This is also true in cases of suspected leak following renal transplant or from other iatrogenic/postsurgical causes. Patients presenting with acute renal failure can be evaluated with renal scintigraphy. A scintigraphic pattern of "relative preservation of flow as compared to function" has been identified as indicative of acute tubular necrosis, which is distinct from other potential causes of acute renal failure, such as nephrotoxicity and in the case of renal transplants, rejection.
 ...
PMID:Renal scintigraphy in the acute care setting. 2341 27

Calcium oxalate (CaOx) crystal deposition within the tubules is often a perplexing finding on renal biopsy of both native and transplanted kidneys. Understanding the underlying causes may help diagnosis and future management. The most frequent cause of CaOx crystal deposition within the kidney is hyperoxaluria. When this is seen in native kidney biopsy, primary hyperoxaluria must be considered and investigated further with biochemical and genetic tests. Secondary hyperoxaluria, for example due to enteric hyperoxaluria following bariatric surgery, ingested ethylene glycol or vitamin C overdose may also cause CaOx deposition in native kidneys. CaOx deposition is a frequent finding in renal transplant biopsy, often as a consequence of acute tubular necrosis and is associated with poorer long-term graft outcomes. CaOx crystal deposition in the renal transplant may also be secondary to any of the causes associated with this phenotype in the native kidney. The pathophysiology underlying CaOx deposition is complex but this histological phenotype may indicate serious underlying pathology and should always warrant further investigation.
Urolithiasis 2020 Oct
PMID:Calcium oxalate crystal deposition in the kidney: identification, causes and consequences. 3271 90