Recovery from Acute Ischaemic Renal Failure is Accelerated by Des-(1–3)-Insulin-Like Growth Factor-1

1994 ◽  
Vol 86 (6) ◽  
pp. 709-714 ◽  
Author(s):  
Ross Clark ◽  
Deborah Mortensen ◽  
Ralph Rabkin
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Growth Factor ◽  
Fractional Excretion ◽  
Insulin Like Growth Factor ◽  
Ischaemic Injury ◽  
Beneficial Effects ◽  
Nitrogen Levels ◽  
Renal Tubular Cells ◽  
Renal Tubular

1. Acute renal failure carries a high risk of morbidity and mortality, so there is a need for agents that minimize renal injury after an insult and that hasten repair. Insulin-like growth factor-1 is mitogenic for renal tubular cells; in normal kidneys it has haemodynamic effects and it is potently anabolic. We tested the theory that insulin-like growth factor-1 may be of use in the treatment of acute renal failure by administering recombinant des-(1–3)-insulin-like growth factor-1, a truncated form of insulin-like growth factor-1, which occurs naturally. Ischaemic renal failure was induced in normal rats by occluding both renal pedicles for 60 min. Then des-(1–3)-insulin-like growth factor-1 (0.8 mg day−1 kg−1) or vehicle was given by subcutaneous minipump for 7 days. The rats were weighed and bled daily and in one experiment were housed in metabolic cages and urine was collected. 2. Des-(1–3)-insulin-like growth factor-1 caused a lower and earlier peak in both serum creatinine and blood urea-nitrogen levels, and a more rapid and complete return toward basal values than in untreated animals. Also des-(1–3)-insulin-like growth factor-1 significantly increased creatinine clearance and reduced fractional excretion of filtered sodium. Besides these beneficial effects on kidney function, des-(1–3)-insulin-like growth factor-1 was anabolic as treated rats gained weight while control rats lost weight. The mortality in control rats was 28% compared with 6% in treated rats. 3. Thus des-(1–3)-insulin-like growth factor-1 accelerated recovery from acute ischaemic injury and may be useful for the treatment of acute renal failure.

scholarly journals The beneficial effects of thyroxine on nephrotoxic acute renal failure in the rat.

1991 ◽  
Vol 1 (11) ◽  
pp. 1236-1240
Author(s):  
U F Michael ◽  
J L Logan ◽  
L A Meeks
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Potassium Dichromate ◽  
Fractional Excretion ◽  
Repair Process ◽  
Acid Extraction ◽  
Sprague Dawley ◽  
Beneficial Effects ◽  
Fractional Excretion Of Sodium ◽  
Renal Tubular

We were able to confirm previous studies demonstrating that administration of thyroxine is capable of ameliorating the severity of acute nephrotoxic renal failure in the rat. Nephrotoxic acute renal failure was induced by the subcutaneous injection of potassium dichromate (6.25 mg/kg) into Sprague-Dawley rats. Twenty-four hours after this injection, rats received an intraperitoneal injection of either thyroxine (80 micrograms/kg body wt) or normal saline. Forty-eight hours after the potassium dichromate injection, renal clearance studies were performed. Inulin clearance was significantly higher in the thyroxine-treated than in the saline-treated acute renal failure rats: 1.12 +/- 0.13 (SEM) mL/g versus 0.75 +/- 0.07 mL/min/g kidney wt (P = 0.025). Thyroxine treatment also effected an increase of p-aminohippuric acid extraction from 0.23 +/- 0.03 to 0.33 +/- 0.02 (P = 0.011) and a decrease in the fractional excretion of sodium from 0.38 +/- 0.21 to 0.11 +/- 0.03% (P = 0.037 by Mann-Whitney U test). In order to investigate one potential mechanism of the beneficial effect of thyroxine we studied renal tubular regeneration in this model of acute renal failure. Renal cortical uptake of labeled thymidine into DNA was significantly increased 48 h after the injection of potassium dichromate, and thyroxine administration further enhanced this repair process: 53.9 +/- 3.6 versus 81.4 +/- 5.3 dpm/200 pg of DNA (P = 0.0033).

Hepatocyte growth factor may function as a renotropic factor for regeneration in rats with acute renal injury

1993 ◽  
Vol 265 (1) ◽  
pp. F61-F69 ◽  
Author(s):  
T. Igawa ◽  
K. Matsumoto ◽  
S. Kanda ◽  
Y. Saito ◽  
T. Nakamura
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Hepatocyte Growth Factor ◽  
Dna Synthesis ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Hepatocyte Growth

Hepatocyte growth factor (HGF), a potent mitogen for mature hepatocytes, possesses mitogenic and morphogenic activities for renal epithelial cells. To examine the renotropic function of HGF, we investigated the expression of HGF mRNA and HGF activity in the rat kidney after acute renal failure. When acute renal failure was induced by ischemia or by HgCl2 administration, a DNA synthesis occurred predominantly in the renal tubular cells located in the outer medulla with a peak at 48 h after the treatments. In both renal injuries, HGF mRNA in the kidney increased markedly, reaching a maximum 6 to 12 h after the treatments. HGF activity in the kidney also increased to three- to fourfold higher level than the normal level at 12 h after ischemic treatment or HgCl2 administration. In situ hybridization and immunohistochemical analysis indicated that both HGF mRNA and HGF protein were expressed in renal interstitial cells, presumably endothelial cells and macrophages, but not in tubular epithelial cells. In addition, HGF activity in the plasma of rats with renal ischemia or HgCl2 administration rapidly increased, reaching a maximum at 6 h after the treatment. One week after these injuries, HGF mRNA and HGF activity reverted to normal levels, and renal tubular cell regeneration ceased. Moreover, intravenous injection of human recombinant HGF into mice with acute renal failure caused by HgCl2 administration stimulated DNA synthesis of renal tubular cells in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)

The Insulin-Like Growth Factor–I Axis in Acute Renal Failure

Renal Failure ◽  
1998 ◽  
Vol 20 (2) ◽  
pp. 343-348 ◽  
Author(s):  
Michael M. Friedlaender ◽  
Fernando C. Fervenza ◽  
Tanny Tsao ◽  
Fay Hsu ◽  
Ralph Rabkin
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Growth Factor ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Growth Factor I

Serum and urinary insulin-like growth factor-1 and tumor necrosis factor in neonates with and without acute renal failure

2002 ◽  
Vol 17 (5) ◽  
pp. 332-336 ◽  
Author(s):  
C. Kornhauser ◽  
Luis-Antonio Dubey ◽  
M.-Eugenia Garay ◽  
Elva-Leticia Pérez-Luque ◽  
Juan-Manuel Malacara ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Insulin Like Growth Factor ◽  
Necrosis Factor

scholarly journals Potential Benefit of Plasma Exchange in Treatment of Severe Icteric Leptospirosis Complicated by Acute Renal Failure

2002 ◽  
Vol 9 (2) ◽  
pp. 482-484 ◽  
Author(s):  
Kai-Chung Tse ◽  
Pok-Siu Yip ◽  
King-Men Hui ◽  
Fu-Keung Li ◽  
Kwok-Yung Yuen ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Plasma Exchange ◽  
Cell Function ◽  
Clinical Manifestations ◽  
Renal Tubular Cell ◽  
Beneficial Effects ◽  
Hemorrhagic Tendency ◽  
Renal Tubular ◽  
Severe Hyperbilirubinemia

ABSTRACT Leptospirosis is a common zoonosis seen worldwide, but it is rare in our locality (Hong Kong). Clinical manifestations of leptospirosis are variable and may range from subclinical infection to fever, jaundice, hemorrhagic tendency, and fulminant hepato-renal failure. Severe hyperbilirubinemia and acute renal failure have been associated with high mortality. We report our experience with a patient who developed severe Weil's syndrome with marked conjugated hyperbilirubinemia and oliguric acute renal failure. These complications persisted despite treatment with penicillin and hemodiafiltration. Plasma exchange was instituted in view of the severe hyperbilirubinemia (970 μmol/liter). This was followed by prompt clinical improvement, with recovery of liver and renal function. The beneficial effects of plasma exchange could be attributed to amelioration of the toxic effects of hyperbilirubinemia on hepatocyte and renal tubular cell function. We conclude that plasma exchange should be considered as an adjunctive therapy for patients with severe icteric leptospirosis complicated by acute renal failure who have not shown rapid clinical response to conventional treatment.

scholarly journals The Growth Hormone and Insulin-Like Growth Factor Axis: Its Manipulation for the Benefit of Growth Disorders in Renal Failure

2001 ◽  
Vol 12 (6) ◽  
pp. 1297-1306 ◽  
Author(s):  
VINCENT ROELFSEMA ◽  
ROSS G. CLARK
Keyword(s):  
Growth Hormone ◽  
Renal Failure ◽  
Growth Factor ◽  
Animal Studies ◽  
Growth Failure ◽  
Growth Disorders ◽  
Insulin Like Growth Factor ◽  
Growth Responses ◽  
Beneficial Effects ◽  
Igf I

Abstract. Renal failure is associated with dramatic changes in the growth hormone/insulin-like growth factor (GH/IGF) axis. In children, this results in growth retardation, which is treated with injections of recombinant human GH (rhGH). Given the many recent advances in the knowledge of the components of the GH/IGF axis, it is timely to review the role of GH in renal failure and to discuss likely new treatments for growth failure. Renal failure is not a state of GH deficiency but a state of GH and IGF resistance, making other approaches to manipulating the GH axis more logical than treatment with rhGH alone. Although in children rhGH is safe, in critically ill adults it can be lethal. As the mechanisms of these lethal actions of rhGH are unknown, caution is advised when using rhGH outside approved indications. In renal failure, an optimal balance between safety and efficacy for growth may be achieved with the use of the combination of rhGH and rhIGF-I, as animal studies have shown synergistic growth responses. However, inhibition of the GH axis, with the use of GH antagonists, is likely to be tested clinically given the beneficial effects of GH antagonists on renal function in animal models of renal disease. Manipulating IGF-I by either administering rhIGF-1 or its binding proteins or increasing IGF-I bioavailability with the use of IGF displacers could prove to be a safer and more effective alternative to the use of rhGH in renal failure. In the future, both rhGH and rhIGF-1 likely will be included in growth-promoting hormone cocktails tailored to correct specific growth disorders.

Insulin-like growth factor I administration in young rats with acute renal failure

2002 ◽  
Vol 17 (12) ◽  
pp. 1005-1012 ◽  
Author(s):  
Alberto Medina ◽  
Marta Fernández-Fuente ◽  
Eduardo Carbajo-Pérez ◽  
Fernando Santos ◽  
Benito Amil ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Growth Factor ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Young Rats ◽  
Growth Factor I

scholarly journals Renal growth hormone—Insulin-like growth factor-I system in acute renal failure

1995 ◽  
Vol 47 (6) ◽  
pp. 1658-1668 ◽  
Author(s):  
Tanny Tsao ◽  
Jin Wang ◽  
Fernando C. Fervenza ◽  
Thanh H. Vu ◽  
Isabella H. Jin ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Growth Factor ◽  
Insulin Like Growth Factor ◽  
Renal Growth ◽  
Factor I ◽  
Growth Factor I

scholarly journals GAMBARAN HITOLOGI GINJAL TIKUS PUTIH (WISTAR) SETELAH PEMBERIAN RIFAMPISIN

2013 ◽  
Vol 1 (1) ◽  
Author(s):  
Indah S. Mappa ◽  
Carla Kairupan ◽  
Lily Loho
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Research Laboratory ◽  
Amycolatopsis Mediterranei ◽  
Treatment Groups ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Tubular Necrosis ◽  
Antibiotic Drug ◽  
Renal Tubular

Abstract: Rifampicyn a bactericidal antibiotic drug of the rifamycin group. The drug is made ​​from semisynthetic compound derived from Amycolatopsis rifamycinica (formerly known as Amycolatopsis mediterranei and Streptomyces mediterranei). Rifampicyn dose of 600 mg / day in humans can cause side effects such as kidney renal insufficiency, acute renal failure, urine output, and the orange-red. This study a imsto look at the white rat renal histological (Wistar) after administration of rifampin. This research was conducted at the Research Laboratory of Integrated Pathology Faculty of Medicine University of Sam Ratulangi Manado. Study using 10 rats (Wistar) consisting of 3 treatment groups. The results showed that the use of rifampicyn at a dose of 5 mg in rats (Wistar) showed vacuole-vacuole in the renal tubular cells, where as the use of rifampicyn at a dose of 8 mg in rats (Wistar) causes acute tubular necrosis. Keywords: Kidney White Rat (Wistar), rifampicyn.  Abstrak: Rifampisin adalah obat antibiotik bakterisida dari kelompok rifamycin. Obat  ini   terbuat  dari  senyawa semisintetik yang berasal dari Amycolatopsis rifamycinica (sebelumnya dikenal sebagai Amycolatopsis mediterranei dan Streptomyces mediterranei). Rifampisin dosis 600 mg/hari pada manusia dapat menyebabkan efek samping terhadap ginjal berupa insufiensi ginjal, gagal ginjal akut, dan pengeluaran urin yang berwarna oranye-kemerahan. Penelitian ini bertujuan untuk melihat gambaran histologi ginjal tikus putih (Wistar) setelah pemberian rifampisin. Penelitian ini dilakukan di Laboratorium Riset Terpadu Patologi Anatomi Fakultas Kedokteran Universitas Sam Ratulangi Manado. Penelitian mengunakan 10 ekor tikus (Wistar) terdiri dari 3 kelompok perlakuan. Hasil penelitian menunjukkan bahwa pengunaan rifampisin dengan dosis 5 mg pada tikus (Wistar) menunjukkan adanya vakuola-vakuola di dalam sel tubulus ginjal, sedangkan pengunaan rifampisin dengan dosis 8 mg pada tikus (Wistar)  menyebabkan terjadinya nekrosis tubular akut. Kata Kunci: Ginjal Tikus Putih (Wistar), Rifampisin.

Rat models for clinical use of insulin-like growth factor I in acute renal failure

1994 ◽  
Vol 266 (6) ◽  
pp. F949-F956 ◽  
Author(s):  
S. B. Miller ◽  
D. R. Martin ◽  
J. Kissane ◽  
M. R. Hammerman
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Growth Factor ◽  
Therapeutic Agent ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Renal Histology ◽  
Igf I ◽  
Growth Factor I ◽  
Short Time

Insulin-like growth factor I (IGF-I) improves kidney function and histopathology, when given within a short time (0.5 or 5 h) after an ischemic renal insult in rats. To examine the effects of IGF-I at times that would be more applicable if it were to be used as a therapeutic agent for acute renal failure in humans, we administered IGF-I to rats 24 h after ischemic injury or prior to the induction of injury (pretreatment). In rats that received IGF-I 24 h postischemia, serum creatinine and blood urea nitrogen (BUN) values were significantly lower during the subsequent 6 days than in vehicle-treated rats, and incorporation of 5-bromo-2'-deoxyuridine into tubular cells of the regenerating cortex, measured 48 h postischemia, was enhanced. When examined 7 days postinjury, kidneys from rats that received IGF-I 24 h postischemia were improved in histopathological appearance compared with kidneys from vehicle-treated animals. Whereas creatinine and BUN values were elevated above baseline in both vehicle and IGF-I-pretreated groups, recovery of normal renal function was accelerated by pretreatment with IGF-I. In addition, although we could detect no differences in histopathology at 24 h postinjury, IGF-I pretreatment resulted in more normal renal histology at 7 days postischemic injury and reduced weight loss after injury. Our data show that IGF-I hastens recovery and accelerates regeneration or repair of damaged epithelia following acute renal failure in rats when administered either 24 h postinjury or prior to induction of acute renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)

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