Acute tubular necrosis treatment

Adverse Effects. The primary problem associated with foscarnet is impaired renal function, including acute tubular necrosis. Hematologic disorders (anemia, granulocytopenia, leukopenia), gastrointestinal disturbances (cramps, nausea, vomiting), and CNS toxicity (confusion, dizziness) may also occur during foscarnet treatment. 

Treatment should be selected based on the grade of kidney dysfunction. In deciding on conservative therapy, hydration must be controlled. Hydration is normalized according to the presence or absence of overhydration and dehydration, although dehydration is rare. When oliguria, hyperpotassemia, and uremia are observed (21% of the patients), dialysis therapy should be considered according to the indication for dialysis therapy in acute tubular necrosis. 

Many patients have non-oliguric acute renal failure, with a good prognosis. However, some patients require dialysis. For treatment, hydration must be controlled, and nonsteroidal anti-inflammatory drugs (NSAIDs) should be avoided if possible. When oliguria is observed, dialysis therapy should be performed, as described for acute tubular necrosis. 

Nephrotoxicity can present as acute tubular necrosis or, more commonly, as gradually evolving non-ohguric renal failure. The time-course of toxicity is variable, but it usually develops only after several days of treatment. Early diagnosis is difficult, since there can be a reduction in glomerular filtration before a significant rise in serum... 

Acute ciclosporin-induced nephrotoxicity, causing reduced renal function, develops within the first month, and includes a dose-related rise in serum creatinine concentrations and hyperkalemia. Fatal acute tubular necrosis has also been noted after very high intravenous doses (SEDA-19, 345). Although it is clinically often difficult to differentiate from acute allograft rejection in renal transplant patients, the alteration in renal function promptly resolves on ciclosporin withdrawal or dosage reduction, and initial acute renal insufficiency is not clearly associated with the development of subsequent chronic renal dysfunction (93). Several conditions, such as pre-existing hypovolemia, concomitant diuretic treatment, or renal artery stenosis, are susceptibility factors. 

Descamps C, Vandenbroucke JM, van Ypersele de Strihou C. Rhabdomyolysis and acute tubular necrosis associated with carbenoxolone and diuretic treatment. BMJ 1977 1(6056) 272. 

Occurrence of acute renal failure from p-lactam treatment may be prevented by early treatment of serious infections, together with maintenance of hemodynamic stability, renal perfusion, and urinary solute excretion. The (3-lactam induced renal failure has a time course comparable to acute tubular necrosis of other origins. While there is no firm evidence that dialysis will speed up renal recovery, clinical stabihty and good nutrition are likely to improve recovery, as it is also the case with other types of renal failure. 

Dutertre JP, Despert E, Jonville AP, Autret E, Nivet H. Acute tubular necrosis during a treatment with Bactrim. Archives francaises de pediatrie. 1991 Jun-Jul 48(6) 441-2. 

Nephrotoxicity of bisphosphonates is a known complication of this compound class, often exacerbated by diseases that compromise renal function, such as multiple myeloma, and by concomitant use of antineo-plastic agents, steroids, and radiation therapy. The first reports of tubulointerstitial damage after treatment with etidronate and clodronate appeared more than 2 decades ago [60]. Subsequently, acute tubular necrosis, focal segmental glomerulosclerosis (FSGS), and granulomatous interstitial nephritis have been reported in renal biopsies from predominantly cancer patients exposed to several bisphosphonates, often at high i.v. doses. 

Markowitz GS, Fine PL, Stack Jl, KunisCL, Radhakrishnan J, Palecki W, Park J, Nasr SEI, Eloh S, Siegel DS,etal.Toxic acute tubular necrosis following treatment with zoledronate (Zometa). Kidney Int 2003 64 281 -289. 

FIGURE 42-2. Suggested treatment algorithm for ICU-acquired oliguric acute renal failure resulting from acute tubular necrosis. 

IFN-P shares 29% amino acid homology with IFN-a and has been used in the treatment of multiple sclerosis. Type 1 interferons (a and P) differ from Type II interferons (y) in biochemical properties, biological function, and receptor specificity. Side effects common to both classes of interferons include chills, fever, rigors, headache, myalgia s, hypotension, nausea, vomiting, anorexia, constipation, fatigue, neutropenia, and elevated transaminases. This constellation of symptoms frequently results in mild to moderate hypotension and volume depletion and could potentially contribute to prerenal azotemia or acute tubular necrosis. 

A. Nephrotoxicity (eg, acute tubular necrosis, proteinuria, and hematuria) may be minimized by adequate hydration, estabiishment of adequate urine flow, avoidance of excessive doses, and iimitation of continuous administration to 5 or fewer days. Laboratory assessment of renai function should be performed daily during treatment for severe intoxication and after the second and fifth days in other cases. 

ARF due to toxic or ischemic injury is the clinical syndrome referred to as acute tubular necrosis common disease with high overall mortality (approximately 50%). Little progress has been made in treatment since the advent of dialysis more than 30 years ago, [7]. Table 7.4 summarizes the known risk factors for ARF, which should always be kept in mind during drug development (especially in clinical trials). 

Renal Effects. Acute nephritis with albuminuria and oliguria, polyuria, and nitrogen retention were observed in individuals after application of a salve that contained potassium chromate. These effects disappeared in individuals who survived. Autopsy of people who died revealed hyperemia and tubular necrosis (Brieger 1920). Acute nephritis with polyuria and proteinuria were also described in a man who was admitted to a hospital with skin ulcers on both hands due to dermal exposure to ammonium dichromate in a planographic printing establishment where he had worked for a few months (Smith 1931). A 49-year-old man with an inoperable carcinoma of the face was treated with chromic acid crystals. Severe nephritis occurred after treatment with the chromium(VI) compound. Urinalysis revealed marked protein in the urine. Death resulted 4 weeks after exposure. A postmortem examination of the kidneys revealed extensive destruction of the tubular epithelium (Major 1922). 

However, appropriate hydration and the sulfhydryl compound mesna are effective in decreasing the urotox-icity of ifosfamide [100, 101]. Less frequently asymptomatic renal functional abnormalities are reported following treatment with ifosfamide when used at a dose below 1.5 gr/m body skin surface [102, 103]. Acute renal failure secondary to tubular necrosis has been described when high-dose therapy [>5 gr/ m2] is administered, especially if patients were treated previously with cisplatin [104,105]. With escalating doses of a 96 hours infusion of ifosfamide, renal toxicity is dose limiting at 18 gr/ m2 [106]. 

Ingestion of large doses of soluble mercuric salts causes acute kidney injury with tubular necrosis and possibly coexisting renal vasospasm [60]. In the 1950 s, when acute treatment with dialysis was not available, the lethal dose of mercuric bichloride, was estimated to range from 2 to 3.5 g [101]. Long-term ingestion of a laxative containing mercurous chloride by two demented patients resulted in renal impairment with... 

Celiptinium is useful in the treatment of metastatic breast cancer and is useful in combination therapy because of minimal hematotoxicity. Acute and chronic renal failures have been detected in patients treated with celiptinium. Acute renal failure is dose dependent, while chronic effects appear to be cumulative in nature. The primary manifestation of celiptinium nephrotoxicity is tubular necrosis with celiptinium-induced lipid peroxidation in proximal tubular cells proposed as the mechanism of toxicity. 

---