Acute Renal Failure after ? Nephrectomy: Histological and Functional Changes

2015 ◽  
pp. 56-63 ◽  
Author(s):  
N. Gretz ◽  
E. Meisinger ◽  
R. Waldherr ◽  
M. Strauch
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Functional Changes

scholarly journals The elderly patient with acute renal failure.

1995 ◽  
Vol 6 (2) ◽  
pp. 144-153
Author(s):  
J Pascual ◽  
F Liaño ◽  
J Ortuño
Keyword(s):  
Elderly Patient ◽  
Renal Failure ◽  
Renal Function ◽  
Acute Renal Failure ◽  
The Elderly ◽  
Functional Changes ◽  
Therapeutic Decisions ◽  
Prognostic Importance ◽  
Work Up ◽  
Aging Kidney

Structural and functional changes observed in the aging kidney predispose the elderly patient to acute renal failure. Up to 36% of the patients with acute renal failure from this institution were over 70 yr, and the literature is full of similar experiences. The elderly patient with abrupt cessation of adequate renal function requires a special work-up in diagnosis and treatment. Prerenal and obstructive causes are of particular interest. Although the question of whether or not age has an independent prognostic importance during an episode of acute renal failure remains debated; when these and other authors compared the outcome of young and old populations with these disorders, a similar evolution was always observed. Age should not be used as a discriminant factor in therapeutic decisions concerning acute renal failure.

Functional Changes in Acute Renal Failure

1955 ◽  
Vol 117 (3) ◽  
pp. 233-237 ◽  
Author(s):  
John P. Merrill
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Functional Changes

Mitochondrial alterations in cisplatin-induced acute renal failure

1986 ◽  
Vol 250 (6) ◽  
pp. F991-F998 ◽  
Author(s):  
J. A. Gordon ◽  
V. H. Gattone
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Mitochondrial Respiration ◽  
Mitochondrial Calcium ◽  
Cellular Injury ◽  
Functional Changes ◽  
Calcium Accumulation ◽  
Mitochondrial Alterations ◽  
Single Intraperitoneal Injection ◽  
Insight Into

The mild reversible nonoliguric form of acute renal failure is perhaps the most common of many nephrotoxic side effects that occur secondary to cisplatin administration. The present studies were undertaken to gain insight into mitochondria alterations and morphological abnormalities underlying this form of renal failure. Following a single intraperitoneal injection of 5.5 mg/kg body wt of cisplatin changes in renal function, mitochondrial respiration, and calcium accumulation were measured serially over a 9-day period. Results indicate that reversible functional changes secondary to cisplatin are accompanied by changes in mitochondrial respiration and calcium accumulation. A decline in state 3 mitochondrial respiration precedes mitochondrial calcium accumulation. However, calcium accumulation begins to recover before mitochondrial respiration. At the peak of functional and biochemical injury morphological damage is extensive, and mitochondria are strikingly aberrant. The results demonstrate that changes in mitochondrial respiration and calcium accumulation occur secondary to cisplatin administration. Both of these effects may play a role in the renal cellular injury induced by cisplatin.

Prior mannitol and furosemide infusion in a model of ischemic acute renal failure

1981 ◽  
Vol 241 (5) ◽  
pp. F556-F564 ◽  
Author(s):  
M. J. Hanley ◽  
K. Davidson
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Acute Renal Failure ◽  
Rabbit Model ◽  
Thick Ascending Limb ◽  
Functional Changes ◽  
Osmotic Water ◽  
Tubular Transport ◽  
Proximal Straight Tubule ◽  
Ischemic Acute Renal Failure

Tubular transport abnormalities have recently been characterized in a rabbit model of ischemic acute renal failure (ARF). These studies demonstrated severe observable morphologic and functional changes in the proximal nephron together with functional changes in the distal nephron. Tubular debris was often produced by perfusion of proximal nephron segments. In the present study, agents used to prevent ARF were tested in this rabbit model of ARF. Rabbits were infused with either 5% body wt 5% manitol or 20 micrograms . kg-1 . min-1 furosemide in 5% body wt normal saline for the 60 min preceding 60 min of total renal ischemia. Mannitol 1) prevented the development of ARF, 2) maintained fluid reabsorption in the proximal convoluted tubule (PCT) (0.59 +/- 0.03 vs. 0.52 +/- 0.1 nl . mm-1 . min-1) and proximal straight tubule (PST) (0.34 +/- 0.05 vs. 0.39 +/- 0.07 nl . mm-1 . min-1), 3) depressed NaCl reabsorption in the cortical thick ascending limb of Henle's loop (TALH), and 4) did not prevent a decrease in ADH-mediated osmotic water flow in the cortical collecting tubule (CCT). Furosemide 1) partially preserved renal function, 2) partially protected the PCT (0.63 +/- 0.05 vs. 0.38 +/- 0.04 nl . mm-1 . min-1) and PST (0.32 +/- 0.04 vs. 0.22 +/- 0.02 nl . mm-1 . min-1), and 3) did not change the transport capacity of the TALH or the ADH response of the CCT. Preservation of proximal nephron integrity was also reflected by the absence of debris formation. There is a direct relation between an agent's ability to protect the functional integrity of the cells of the proximal nephron and its ability to preserve renal function.

Acute renal failure in zebrafish: a novel system to study a complex disease

2005 ◽  
Vol 288 (5) ◽  
pp. F923-F929 ◽  
Author(s):  
Dirk M. Hentschel ◽  
Kwon Moo Park ◽  
Lucia Cilenti ◽  
Antonis S. Zervos ◽  
Iain Drummond ◽  
...  
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Acute Renal Failure ◽  
Complex Disease ◽  
Genetic Manipulation ◽  
Specific Inhibitor ◽  
Clinical Syndrome ◽  
Novel Therapies ◽  
Functional Changes ◽  
Larval Zebrafish

Acute renal failure (ARF) is characterized by a very high mortality essentially unchanged over the past 40 years. Simple vertebrate models are needed to improve our understanding of ARF and facilitate the development of novel therapies for this clinical syndrome. Here, we demonstrate that gentamicin, a commonly used nephrotoxic antibiotic, causes larval zebrafish to develop ARF characterized by histological and functional changes that mirror aminoglycoside toxicity in higher vertebrates and inability of zebrafish to maintain fluid homeostasis. We developed a novel method to quantitate renal function in larval zebrafish and demonstrate a decline in glomerular filtration rate after gentamicin exposure. The antineoplastic drug cisplatin, whose use in humans is limited by kidney toxicity, also causes typical histological changes and a decline in renal function in larval zebrafish. A specific inhibitor of Omi/HtrA2, a serine protease implicated in cisplatin-induced apoptosis, prevented renal failure and increased survival. This protective effect was confirmed in a mouse model of cisplatin-induced nephrotoxicity. Therefore, zebrafish provides a unique model system, amenable to genetic manipulation and drug screening, to explore the pathophysiology of ARF and establish novel therapies with potential use in mammals.

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