Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal artery thrombosis after blunt trauma presented without other injury, without external signs of trauma, and without hematuria in the case reported. Review of 65 cases from the literature showed that flank and epigastric pain and proteinuria are usually present. Renal artery thrombosis following blunt trauma has usually been diagnosed too late to salvage the kidney. Nephrectomy is performed for ileus, fever, and pain caused by the necrotic kidney, or for hypertension. Ideally, rapid diagnosis by intravenous pyelogram and arteriography and early surgical intervention should allow revascularization and renal salvage before permanent parenchymal damage has occurred. The cases reviewed showed that successful revascularization without hypertension could be achieved 12 hours after injury. Patent small collateral vessels as well as incomplete or gradual renal artery occlusion may prolong renal salvage time.
 ...
PMID:Renal artery thrombosis following blunt trauma. 739 14

We encountered four adult patients who received renal transplants from young children < 36 months of age, each of whom developed severe hypertension, heavy proteinuria, and progressive renal failure. Biopsies disclosed glomerular sclerosis with crescents in three patients and mesangial expansion in one. We thus analyzed our experience with 74 adults who received grafts from donors < or = 10 years of age and compared the results to those of 804 patients who were transplanted with kidneys from donors > 10 years of age. A Kaplan-Meier analysis revealed that graft survival was significantly worse in patients receiving grafts from younger, compared to older donors. This difference was apparent in patients treated either with or without cyclosporine. A subanalysis comparing patients with donor grafts aged < or = 5 or 6-10 years revealed a further adverse age-related effect. Renal artery thrombosis and recurrent or de novo biopsy-proven glomerulonephritis were more common in patients receiving grafts from younger donors, while graft failure from rejection actually appeared less common. We conclude that severe hypertension and resultant glomerular hyperperfusion promoted glomerulosclerosis and crescent formation in our patients. Our results have caused us to pursue a more conservative approach towards transplanting grafts from donors aged < or = 10 years into adult recipients.
 ...
PMID:Kidneys from pediatric donors: risk versus benefit. 773 81

Acute renal failure in the newborn is a common problem and is typically classified as prerenal, intrinsic renal disease including vascular insults, and obstructive uropathy. In the newborn, renal failure may have a prenatal onset in congenital diseases such as renal dysplasia with or without obstructive uropathy and in genetic diseases such as autosomal recessive polycystic kidney disease. Acute renal failure in the newborn is also commonly acquired in the postnatal period because of hypoxic ischemic injury and toxic insults. Nephrotoxic acute renal failure in newborns is usually associated with aminoglycoside antibiotics and nonsteroidal anti-inflammatory medications used to close a patent ductus arteriosis. Alterations in renal function occur in approximately 40% of premature newborns who have received indomethacin and such alterations are usually reversible. Renal artery thrombosis and renal vein thrombosis will result in renal failure if bilateral or if either occurs in a solitary kidney. Cortical necrosis is associated with hypoxic/ischemic insults due to perinatal anoxia, placenta abruption and twin-twin or twin-maternal transfusions with resultant activation of the coagulation cascade. As in older children, hospital acquired acute renal failure is newborns is frequently multifactorial in origin. Although the precise incidence and prevalence of acute renal failure in the newborn is unknown, several studies have shown that acute renal failure is common in the neonatal intensive care unit. Recent interesting studies have demonstrated that some newborns may have genetic risks factors for acute renal failure. Once intrinsic renal failure has become established, management of the metabolic complications of acute renal failure continues to involve appropriate management of fluid balance, electrolyte status, acid-base balance, nutrition and the initiation of renal replacement therapy when appropriate. Renal replacement therapy may be provided by peritoneal dialysis, intermittent hemodialysis, or hemofiltration with or without a dialysis circuit. The preferential use of hemofiltration by pediatric nephrologists is increasing while the use of peritoneal dialysis is decreasing except for neonates and small infants. Peritoneal dialysis has been a major modality of therapy for acute renal failure in the neonate when vascular access may be difficult to maintain. In the newborn, the prognosis and recovery from acute renal failure is highly dependent upon the underlying etiology of the acute renal failure. Factors that are associated with mortality include multiorgan failure, hypotension, need for pressors, hemodynamic instability, and need for mechanical ventilation and dialysis. The mortality and morbidity of newborns with acute renal failure is much worse in neonates with multiorgan failure. Newborns who have suffered substantial loss of nephrons as may occur in cortical necrosis are at risk for late development of renal failure after apparent recovery from the initial insult. Similarly, hypoxic/ischemic and nephrotoxic injury to the developing kidney can result is decreased nephron number. Newborns with acute renal failure need life-long monitoring of their renal function, blood pressure, and urinalysis. Typically, the late development of chronic renal failure will first becomes apparent with the development of hypertension, proteinuria, and eventually an elevated blood urea nitrogen and creatinine.
 ...
PMID:Acute renal failure in the newborn. 1520 Feb 50