[Environmental factors and tubulointerstitial nephropathy : the paradigm of «chronic interstitial nephritis in agricultural communities» (CINAC)].

Chronic Interstitial Nephritis in Agricultural Communities (CINAC) represents a major public health challenge, primarily affecting young to middle-aged agricultural workers. Clinically, CINAC is characterized by low-grade proteinuria, a bland urinary sediment, and rapidly progressive renal failure. Kidney biopsies disclose large dysmorphic lysosomes containing electron-dense non-membrane aggregates in proximal tubular cells. Although the disease was long attributed to recurrent episodes of dehydration, its pathophysiology is now recognized as more complex. Indeed, the heat-stress hypothesis alone does not adequately explain the heterogeneous geographic distribution of CINAC. Converging epidemiological, environmental, and toxicological evidence suggests a significant role for chronic exposure to pesticides. Several classes of agrochemicals experimentally demonstrated cumulative nephrotoxicity, involving oxidative stress, tubular apoptosis, and mitochondrial and lysosomal dysfunction. The frequent detection of pesticide residues in drinking water and soils within endemic regions indicates chronic low-dose exposure, sometimes independent of direct occupational handling. Heat stress likely acts as a cofactor, amplifying toxicity through dehydration, reduced renal perfusion, and intratubular concentration of toxins. Overall, CINAC appears to result from a multifactorial etiology dominated by exposure to agrochemical mixtures, underscoring the need for integrated and sustainable prevention strategies including depollution and/or reversed osmosis of drinkable water.