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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Radionuclide scintigraphy of the renal transplant has assumed an important role in disclosing the complications that beset this life-prolonging procedure. Renal ischemia, whether caused by mechanical obstruction of the blood vessels or ureter or immunological rejection, can be detected by qualitative and quantitative perfusion studies using 99mTc-complexes such as pertechnetate, glucoheptonate and DTPA. Similarly, parenchymal agents such as radiohippurate and 99mTc-DTPA can be quantitated for uptake and their drainage patterns monitored to reveal possible underlying obstructive uropathy and urine extravasation. The literature is replete with mathematical strategems for quantitating perfusion and parenchymal transit of the tracers, but none are truly specific enough to be diagnostic of a given cause of renal ischemia. Serial quantitative radionuclide studies should be obtained during the first 2-3 wk after transplantation with the view of noting an improvement or deterioration of the quantitation parameters as a guage of progress. A deterioration may anticipate biochemical manifestations by 24-48 hr, but it is not specific and must be interpreted in light of the clinical circumstances or necessitate invasive procedures for a definitive diagnosis.
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PMID:Renal transplant evaluation. 676 Apr 1

In the present review, the possibilities of ergometric and pharmacological "intervention" with a view to improving the validity of scintirenography are reported. Exercise renography at present does not have a defined role in clinical routine. This procedure, however, gives additional information in hypertensive patients with respect to renal ischemia. Captopril scintirenography can be recommended as a screening test for renovascular hypertension. Furosemide-"intervention" differentiates between obstructive uropathy and dilatation of renal collecting system without obstruction. This is true especially in newborns with congenital abnormalities of the upper urinary tract, in order to stratify these young patients for surgical or conservative treatment.
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PMID:[Intervention in nuclear medicine kidney diagnosis]. 784 1

Renal tubular dysgenesis (RTD), with hypoplasia especially of renal proximal convoluted tubules and clinical neonatal anuria or oliguria, has been reported as a congenital familial (autosomal recessive) disease, variably with features of oligohydramnios, Potter syndrome, or pulmonary hypoplasia. A similar tubular lesion due to antenatal tubular atrophy has been reported for conjoined twins with twin-twin transfusion syndrome or acardia and in infants of mothers given antihypertensive agents, including angiotensin-converting enzyme (ACE) inhibitors, during pregnancy, and it has been seen as a unilateral lesion in young infants with renal artery stenosis due to arteritis or medial arterial calcinosis. The renal tubular changes in RTD are very like those of the "endocrine kidney" in experimental animals and resemble those of the renal tubular atrophy of end-stage kidney diseases such as glomerulonephritis, tubulointerstitial kidney disease, obstructive uropathy/pyelonephritis, graft rejection of transplanted kidneys, or the renal parenchymal changes seen with protracted dialysis therapy. Labeled lectins that differentially mark proximal convoluted, distal convoluted and connecting, and collecting tubules showed no distinctive differences in staining patterns of the hypoplastic renal tubules of infants and children with RTD, postnatal renal artery obstruction, or the various types of end-stage renal disease with the lectins used (PNA, GSLI, UEA, and LTA). The findings suggest that the renal tubular changes in some if not all the conditions studied are the result of renal ischemia. The reported familial RTD with hypernephronic nephromegaly may be a specific disorder, but other forms could reflect renal ischemia acquired in utero or in early or later postnatal life.
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PMID:Labeled lectin studies of renal tubular dysgenesis and renal tubular atrophy of postnatal renal ischemia and end-stage kidney disease. 815 24

Obstructive uropathy can cause irreversible renal damage. It has been hypothesized that elevated hydrostatic pressure within renal tubules and/or renal ischemia contributes to cellular injury following obstruction. However, these assaults are essentially impossible to isolate in vivo. Therefore, we developed a novel pressure system to evaluate the isolated and coordinated effects of elevated hydrostatic pressure and ischemic insults on renal cells in vitro. Cells were subjected to: (1) elevated hydrostatic pressure (80 cm H(2)O); (2) ischemic insults (hypoxia (0% O(2)), hypercapnia (20% CO(2)), and 0 mM glucose media); and (3) elevated pressure + ischemic insults. Cellular responses including cell density, lactate dehydrogenase (LDH) release, and intracellular LDH (LDH(i)), were recorded after 24 h of insult and following recovery. Data were analyzed to assess the primary effects of ischemic insults and elevated pressure. Unlike pressure, ischemic insults exerted a primary effect on nearly all response measurements. We also evaluated the data for insult interactions and identified significant interactions between ischemic insults and pressure. Altogether, findings indicate that pressure may sub-lethally effect cells and alter cellular metabolism (LDH(i)) and membrane properties. Results suggest that renal ischemia may be the primary, but not the sole, cause of cellular injury induced by obstructive uropathy.
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PMID:Investigating the role of ischemia vs. elevated hydrostatic pressure associated with acute obstructive uropathy. 1938 12