Pathophysiological roles of Ca2+ overload via the Na+/Ca2+ exchanger and endothelin-1 overproduction in ischaemia/reperfusion-induced acute renal failure

2002 ◽  
Vol 103 (s2002) ◽  
pp. 389S-392S ◽  
Author(s):  
Yasuo MATSUMURA ◽  
Junji YAMASHITA ◽  
Satomi KITA ◽  
Takahiro IWAMOTO ◽  
Masaya OGATA ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Tubular Epithelium ◽  
Wild Type ◽  
Endothelin 1 ◽  
Tubular Necrosis ◽  
Reverse Mode ◽  
Ischaemia Reperfusion ◽  
Pathophysiological Role ◽  
The Difference

Using Na+/Ca2+ exchanger (NCX1)-deficient mice, the pathophysiological role of Ca2+ overload via the reverse mode of the Na+/Ca2+ exchanger in ischaemia/reperfusion-induced renal injury was investigated. Since NCX1-/- homozygous mice die of heart failure before birth, we utilized NCX1+/- heterozygous mice. The ischaemia/reperfusion-induced renal dysfunction in heterozygous mice were significantly attenuated compared with cases in wild-type mice. Also, histological renal damage such as tubular necrosis and proteinaceous casts in tubuli in heterozygous mice were much less than that in wild-type mice. Ca2+ deposition in necrotic tubular epithelium was observed more markedly in wild-type than in heterozygous mice. The increase in renal endothelin-1 (ET-1) content was significantly greater in wild-type than in heterozygous mice, and this reflected the difference in immunohistochemical ET-1 localization in necrotic tubular epithelium. We conclude that Ca2+ overload via the reverse-mode of Na+/Ca2+ exchange, followed by renal ET-1 overproduction, plays an important role in the pathogenesis of ischaemia/reperfusion-induced acute renal failure.

Oestrogen protects against ischaemic acute renal failure in rats by suppressing renal endothelin-1 overproduction

2002 ◽  
Vol 103 (s2002) ◽  
pp. 434S-437S ◽  
Author(s):  
Masanori TAKAOKA ◽  
Mikihiro YUBA ◽  
Toshihide FUJII ◽  
Mamoru OHKITA ◽  
Yasuo MATSUMURA
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Acute Renal Failure ◽  
Renal Dysfunction ◽  
Tissue Injury ◽  
Male Rats ◽  
Left Renal Artery ◽  
Protective Effects ◽  
Endothelin 1 ◽  
Ischaemia Reperfusion

We investigated whether the treatment with 17β-oestradiol has renal protective effects in male rats with ischaemic acute renal failure (ARF). We also examined if the effect of 17β-oestradiol is accompanied by suppression of enhanced endothelin-1 production in postischaemic kidneys. Ischaemic ARF was induced by clamping the left renal artery and vein for 45min followed by reperfusion, 2 weeks after contralateral nephrectomy. Renal function parameters such as blood urea nitrogen, plasma creatinine and creatinine clearance were measured to test the effectiveness of the steroid hormone. Renal function in ARF rats markedly decreased 24h after reperfusion. The ischaemia/reperfusion-induced renal dysfunction was dose-dependently improved by pretreatment with 17β-oestradiol (20 or 100µg/kg, intravenously). Histopathological examination of the kidney of untreated ARF rats revealed severe lesions, such as tubular necrosis, proteinaceous casts in tubuli and medullary congestion, all of which were markedly improved by the higher dose of 17β-oestradiol. In addition, endothelin-1 content in the kidney after the ischaemia/reperfusion increased significantly by approx. 2-fold over sham-operated rats, and this elevation was dose-dependently suppressed by the 17β-oestradiol treatment. These results suggest that oestrogen exhibits protective effects against renal dysfunction and tissue injury induced by ischaemia/reperfusion, possibly through the suppression of endothelin-1 overproduction in postischaemic kidneys.

scholarly journals Renal involvement in human rabies: clinical manifestations and autopsy findings of nine cases from northeast of Brazil

2005 ◽  
Vol 47 (6) ◽  
pp. 315-320 ◽  
Author(s):  
Elizabeth De Francesco Daher ◽  
Geraldo Bezerra da Silva Júnior ◽  
Marúsia Thomaz Ferreira ◽  
Fernando Antonio de Sousa Barros ◽  
Tiago Magalhães Gurgel ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Renal Involvement ◽  
Clinical Manifestations ◽  
Signs And Symptoms ◽  
Hemodynamic Instability ◽  
Human Rabies ◽  
Tubular Necrosis ◽  
Post Mortem Findings ◽  
Histopathologic Findings

A retrospective study was conducted in nine patients with rabies admitted to a hospital of Fortaleza, Brazil. Autopsy was performed in all cases. The ages ranged from three to 81 years and six were males. They all were bitten by dogs. The time between the accident and the hospital admission ranged from 20 to 120 days (mean 45 ± 34 days). The time until death ranged from one to nine days (mean 3.3 ± 5.5 days). The signs and symptoms presented were fever, hydrophobia, aerophobia, agitation, disorientation, dyspnea, sialorrhea, vomiting, oliguria, sore throat, pain and hypoesthesia in the site of the bite, headache, syncope, cough, hematemesis, mydriasis, hematuria, constipation, cervical pain and priapism. In three out of six patients, there was evidence of acute renal failure, defined as serum creatinine > 1.4 mg/dL. The post-mortem findings in the kidneys were mild to moderate glomerular congestion and mild to intense peritubular capillary congestion. Acute tubular necrosis was seen in only two cases. This study shows some evidence of renal involvement in rabies. Histopathologic findings are nonspecific, so hemodynamic instability, caused by autonomic dysfunction, hydrophobia and dehydration must be responsible for acute renal failure in rabies.

scholarly journals An evaluation of antioxidant effects on recovery from postischemic acute renal failure.

1994 ◽  
Vol 4 (8) ◽  
pp. 1588-1597
Author(s):  
R A Zager ◽  
S M Fuerstenberg ◽  
P H Baehr ◽  
D Myerson ◽  
B Torok-Storb
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Dna Fragmentation ◽  
Proliferating Cell Nuclear Antigen ◽  
Antigen Expression ◽  
Nuclear Antigen ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tubular Necrosis ◽  
Proliferating Cell

Xanthine oxidase (XO) activity and hydroxyl radical (.OH) formation are widely proposed mediators of renal reperfusion injury, potentially altering the severity of, and recovery from, postischemic acute renal failure. The goal of this study was to ascertain whether combination XO inhibitor (oxypurinol) and .OH scavenger (Na benzoate) therapy, given at the time of renal ischemia, alters the extent of: (1) tubular necrosis and filtration failure; (2) DNA fragmentation/apoptosis (assessed in situ by terminal deoxynucleotidyl transferase reactivity); (3) early tubular regenerative responses (proliferating cell nuclear antigen expression; (3H)thymidine incorporation); and (4) the rate and/or degree of functional and morphologic repair. The effects of XO inhibition, .OH scavengers, and "catalytic" iron (FeSO4) on human proximal tubular cell proliferation in vitro were also assessed with a newly established cell line (HK-2). Male Sprague-Dawley rats were subjected to 35 min of bilateral renal arterial occlusion with or without oxypurinol/benzoate therapy. These agents did not alter the extent of tubular necrosis or filtration failure, proliferating cell nuclear antigen expression or thymidine incorporation, or the rate/extent of renal functional/morphologic repair. DNA fragmentation did not precede tubular necrosis, and it was unaffected by antioxidant therapy. By 5 days postischemia, both treatment groups demonstrated regenerating epithelial fronds that protruded into the lumina. These structures contained terminal deoxynucleotidyl transferase-reactive, but morphologically intact, cells, suggesting the presence of apoptosis. Oxypurinol and .OH scavengers (benzoate; dimethylthiourea) suppressed in vitro tubular cell proliferation; conversely, catalytic Fe had a growth-stimulatory effect. These results suggest that: (1) XO inhibition/.OH scavenger therapy has no discernible net effect on postischemic acute renal failure; (2) DNA fragmentation does not precede tubular necrosis, suggesting that it is not a primary mediator of ischemic cell death; and (3) antioxidants can be antiproliferative for human tubular cells, possibly mitigating their potential beneficial effects.

scholarly journals Acute Renal Failure in a Tertiary Care Center in Nepal

2005 ◽  
Vol 44 (158) ◽  
Author(s):  
Sudha Khakurel ◽  
P R Satyal ◽  
R K Agrawal ◽  
P K Chhetri ◽  
R Hada
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Bacillary Dysentery ◽  
Care Center ◽  
Tertiary Care ◽  
Acute Interstitial Nephritis ◽  
Female Age ◽  
Tubular Necrosis ◽  
Common Causes ◽  
Urate Nephropathy

From July 1998 to July 1999, 45 cases of acute renal failure were treated at Bir Hospital, Kathmandu. Outof which 24 were male and 21 were female. Age ranged from 11 months to 84 years with mean age being 35years and 9 cases were below 10 years.Four cases with pre-renal azotaemia and twenty five cases of acute tubular necrosis (ATN) accounted for64% of all cases. These were due to gastroenteritis 10, sepsis 6, post surgical 1, trauma 1 and obstreticalcomplications 5. Multiple hornet stings were responsible for acute renal failure in 3 cases, acute urate nephropathy in 1 case and miscellaneous causes in 2 cases.Glomerulonephritis / vasculitis accounted for 17.7%, acute interstitial nephritis 4.4%, haemotytic uraemicsyndrome (HUS) 6.6%, and post renal azotaemia in 6.6% of all cases. Mean serum creatinine was 8 mg/dl,mean blood urea 190 mg/dl. Eight cases were treated only conservatively, eighteen received haemodialysis,fourteen received peritoneal dialysis, three received both and two refused for dialysis. Average duration ofhospital stay was 13.6 days. Out of the forty-five cases twenty-nine recovered normal renal function, tenexpired, two recovered partially, two progressed to chronic renal failure and two left against medical advice.Overall mortality was 22.2%.Common causes of acute renal failure in our setting were gastroenteritis (22%) and sepsis (20%). HUS wasexclusively seen in children following bacillary dysentery. Multiple hornet stings is an important cause ofacute renal failure in our country.

Acute Tubular Necrosis: Diagnosis, Treatment, and Nursing Implications

1992 ◽  
Vol 3 (3) ◽  
pp. 688-697
Author(s):  
Sara Douglas
Keyword(s):  
At Risk ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Critical Care ◽  
Acute Tubular Necrosis ◽  
Early Recognition ◽  
Recovery Phase ◽  
Vital Role ◽  
Laboratory Findings ◽  
Tubular Necrosis

Acute tubular necrosis (ATN) is the most common cause of acute renal failure. Early recognition of patients who are at risk for ATN can prevent or improve the course of ATN. Acute renal failure is classified as prerenal, intrinsic, or postrenal disease. ATN is classified as a type of intrinsic renal disease. The clinical course of ATN is divided into the renal failure phase, diuretic phase, and recovery phase, with each phase having distinct symptoms and laboratory findings. Diagnosis of ATN often is complicated and confusing; understanding of laboratory findings can facilitate the critical care nurse’s ability to assess those at risk for ATN. The care and treatment of the patient with ATN is complicated, and specific treatments are discussed in detail. The critical care nurse can play a vital role in identifying the patient at risk, preventing the development of ATN in those at risk, and providing appropriate care for those who develop ATN

The Role of Tubular Necrosis in the Pathophysiology of Acute Renal Failure

Nephron ◽  
1976 ◽  
Vol 17 (3) ◽  
pp. 204-214 ◽  
Author(s):  
Chen H. Hsu ◽  
Theodore W. Kurtz ◽  
John M. Weller
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Tubular Necrosis

scholarly journals Management of Acute Renal Failure

1972 ◽  
Vol 1 (1) ◽  
pp. 65-69 ◽  
Author(s):  
J. M. Hayes
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Acute Tubular Necrosis ◽  
Urinary Tract Obstruction ◽  
Renin Angiotensin System ◽  
Sodium Concentration ◽  
Therapeutic Trial ◽  
Angiotensin System ◽  
Tubular Necrosis ◽  
Occlusive Vascular Disease

Acute renal failure has oliguria and uraemia as its cardinal manifestations. The syndrome may be due to acute tubular necrosis, glomerulonephritis, urinary tract obstruction and occlusive vascular disease. The renal damage due to acute tubular necrosis is of uncertain aetiology. Renal cortical ischaemia and depression of glomerular filtration rate are important in the pathogenesis. Activation of the renin-angiotensin system and glomerular coagulation may prove to be important in these changes. The differentiation between reversible oliguria and established renal failure is generally accomplished on clinical grounds and the response to a therapeutic trial of mannitol. Measurement of urinary sodium concentration and osmolality are valuable adjuncts. The keystone of management is the prevention of symptomatic uraemia. Infection and haemorrhage have now replaced pulmonary oedema and hyperkalaemia as the major causes of death. The mortality rate remains high in acute tubular necrosis and a significant mortality occurs in the diuretic phase.

IgA Nephropathy: Acute Renal Failure, Acute Tubular Necrosis, and Features of Postinfectious Acute Glomerulonephritis

Renal Failure ◽  
1992 ◽  
Vol 14 (4) ◽  
pp. 533-539 ◽  
Author(s):  
Helga Maria Mazzarolo-Cruz ◽  
Décio de Oliveira Penna ◽  
Luis Balthazar Saldanha ◽  
Elza Hissako Kanashiro ◽  
Jenner Cruz ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Iga Nephropathy ◽  
Acute Tubular Necrosis ◽  
Acute Glomerulonephritis ◽  
Tubular Necrosis

scholarly journals NEPHROTOXICITY ATTRIBUTED TO MEGLUMINE ANTIMONIATE (GLUCANTIME) IN THE TREATMENT OF GENERALIZED CUTANEOUS LEISHMANIASIS

1999 ◽  
Vol 41 (1) ◽  
pp. 33-37 ◽  
Author(s):  
M.L.O. RODRIGUES ◽  
R.S. COSTA ◽  
C.S. SOUZA ◽  
N.T. FOSS ◽  
A.M.F. ROSELINO
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Side Effects ◽  
Serum Creatinine ◽  
Cutaneous Leishmaniasis ◽  
Urine Osmolarity ◽  
Hepatic Enzyme ◽  
Meglumine Antimoniate ◽  
Tubular Necrosis ◽  
Electrocardiographic Abnormalities

Background: Pentavalent antimonials have became of basic importance for the treatment of leishmaniasis. Their most severe side effects have been reported to be increased hepatic enzyme levels and electrocardiographic abnormalities. Nephrotoxicity has been rarely related. Observations: We report a case of generalized cutaneous leishmaniasis involving a 50-year old male patient who was submitted to treatment with meglumine antimoniate (Glucantime). He developed acute renal failure (ARF) due to acute tubular necrosis (ATN), followed by death after receiving a total of 53 ampoules of Glucantime. Conclusions: The treatment with Glucantime was responsible by ARF diagnosed in this patient. The previous urine osmolarity and serum creatinine levels were normal and the autopsy showed ATN. It should be pointed out if ARF may also be explained by massive deposits of immunocomplexes by leishmania antibodies and antigens due to the antigenic break by the antimonial compound, since our patient presented countless lesions covering the entire tegument, similar to the Hexheimer phenomenon, but at the autopsy no glomerular alterations were seen.

Sign in / Sign up

Export Citation Format

Share Document