Alpha 1‑microglobulin (α1‑M) is a low molecular weight, pH stable glycoprotein. It has a molar mass of 30000 daltons and is synthesized by the hepatocytes and lymphocytes. It is almost entirely filtered in the glomeruli with approximately 99.8 % of the re‑absorption and catabolism taking place in the proximal tubules. Increased excretion of α1‑microglobulin in tubular proteinuria is indicative of reduced tubular re - absorption under normal glomerular filtration conditions. This form of proteinuria is typical for chronic interstitial nephropathy and for acute and chronic tubular damage caused by endogenous and exogenous tubular toxins. In renal failure, the plasma levels of this microprotein increase from an early stage. The resultant protein hyperfiltration in the residual nephron causes increased renal excretion as re‑absorption capacity is exceeded (overflow proteinuria). α1‑Microglobulin can be used as a marker for the diagnosis of tubulo‑interstitial nephropathy, for example, at an early stage or rule it out with a high degree of certainty; the detection limit is approximately 10‑20 mg/L (333‑666 nmol/L). Acute and chronic forms of tubular insufficiency (all forms of primary and secondary Fanconi syndrome), heavy metal intoxication, nephrotoxic side‑effects of pharmaceuticals, and rejection reactions following kidney transplantation can also be excluded