Experimental Porcine Nephropathy: Changes of Renal Function and Structure Perorally Induced by Crystalline Ochratoxin A

Abstract

Experimental porcine nephropathy: Changes of renal function and structure perorally induced by crystalline ochratoxin A. Acta path. microbiol. scand. Sect. A, 84: 429-434, 1976. Nine pigs were fed crystalline ochratoxin A in amounts corresponding to a feed level of 1 mg per kg for 3 months. The only observable lesion developed was a kidney damage, identical to the naturally occurring porcine nephropathy. The changes of renal function was characterized by impairment of proximal tubular function, indicated by a decrease of the ratio ?'mPAH/C,,,, of the ability to concentrate urine, and by an increased urinary excretion of glucose. The decrease of the ratio 1mpAH/CI,, is correlated with time of exposure to ochratoxin A. The changes of renal structure were characterized by degeneration of the proximal tubules, leading to tubular atrophy accompanied by interstitial fibrosis. At the end of the experiment the kidney, liver, adipose and muscular tissue of the slaughtered pigs contained sizable amounts of ochratoxin A residues. As the pigs would have passed the meat inspection this represents a possible health problem. T h e changes observed in this study are identical to those observed by feeding to pigs grains naturally contaminated with ochratoxin A.

Complex etiology and pathology of mycotoxic nephropathy in South African pigs

“…The amount of OTA in South African feeds (70-80 μg/ kg) from farms with nephropathy problems was significantly less than that presented as the explanation for Danish mycotoxic porcine nephropathy (MPN) (Krogh 1976;Krogh et al 1974). It seems, therefore, that South African porcine nephropathy may have a multitoxic aetiology because it cannot be explained by the concentration of OTA alone, and the conventional explanation appropriate for northern latitudes does not seem to apply.…”

A risk assessment of dietary Ochratoxin a in the United States

“…OTA has been shown, in a variety of animal studies, to cause renal cancer and lifetime exposure to OTA induced renal adenomas or carcinomas in male Fisher-344 rats (NTP 1989). OTA can also cause decreased kidney function at just 8 μg/kg bw/day in female swine (Krogh et al 1974). While the renal system is the main target for OTA toxicity, adverse effects have been observed in other organs; such as cardiac and hepatic histological abnormalities (Hagelberg et al 1989), gastro-intestinal tract and lymphoid tissue lesions, intestinal fragility and kidney lesions (Elling et al 1975), and immunotoxic effects (Bondy and Pestka 2000).…”

A review of potential contaminants in Australian livestock feeds and proposed guidance levels for feed

“…Australian broiler chickens (3 weeks of age) fed 1 mg/kg for 5 weeks were not adversely affected (Reichmann et al 1982). Other studies have reported reduced growth and also reduced egg production in chickens exposed to 0.5-1 mg/kg feed (Huff et al 1975;Krogh et al 1976;Prior and Sisodia 1978;Page et al 1980). A guidance level of 0.1 mg/kg DM is suggested for poultry.…”