Balkan nephropathy is a type of degenerative, familial, slowly progressive chronic tubulointerstitial disease that may lead to carcinomas of the renal pelvis or upper urethra. The disease is endemic to the Balkan countries like Bosnia and Herzegovina, Romania, Serbia, Croatia, and Bulgaria.
Balkan nephropathy is clinically silent initially and occurs three times more frequently in women than men. Affected individuals are usually farmers. First symptoms are nonspecific , occurring usually after the patient turns 30 years old and consists of weakness, anorexia, nausea, vomiting, headache, dizziness, somnolence, muscular spasms, dyspepsia, pale skin with copper-brown discoloration of the palms and soles, weight loss, episodes of macrohematuria and mild, non-characteristic pain in the lumbar area. Blood pressure remains normal in incipient phases and becomes elevated later during illness evolution. Symptoms of chronic kidney disease (uremic syndrome) become apparent as Balkan nephropathy progresses  . Dysuria and fever are absent. Peripheral edema is seldom seen and is due to hydroelectrolytic disturbances. Working capacity is preserved for a long time. Patients with prolonged disease evolution present with urothelial tumors or signs of chronic renal failure: pollakyuria, polydipsia, and nocturia.
Tubular type proteinuria involving albumin and β2-microglobulin is initially intermittent and not accompanied by decreased serum protein levels but later becomes permanent. It is usually less than 0.5 g/24 hours. Urine concentration ability is gradually lost and followed by a decrease in the glomerular filtration rate  . Urinary sediment detects red, white blood cells  and tumor cells if the disease has become complicated by a urothelial tumor . Bacteriuria, glycosuria, enzymuria, and aminoaciduria (hydroxyprolinuria) have been described. Normo- or hypochromic normocytic hypo regenerative anemia is present from the initial stages of the disease and is more severe than expected based on glomerular filtration rate reduction. It is caused by urinary or digestive losses, impaired erythropoietin synthesis, and hemolysis. The erythrocyte sedimentation rate is elevated. Complement, as well as anti-tubular basal membrane and anti-glomerular basal membrane antibodies levels, remain normal. High values of urinary leucine aminopeptidase activity have been described. Tubular dysfunction leads to salt wasting, abnormal ammonia, phosphate and uric acid excretion and urine acidification abnormalities.
Ultrasonography reveals progressive, symmetrical kidney atrophy   due to sclerosis and high echo density of the renal pelvis and parenchyma. Histology demonstrates the substratum of these findings: interstitial and periglomerular fibrosis, glomerular lesions of the endothelial and mesangial proliferative type or micro cysts. Tubular epithelium may be dystrophic or atrophic, may be affected by hydroprotidic de-generescence or pseudo cystic dilatation. Vascular lesions consist of intimal fibrous hyperplasia or intimal fibrosis and arterial hyalinosis.
Radiography and other imaging methods may reveal carcinomas that usually involve the upper ureter or renal pelvis . Tumors may also be encountered in the urinary bladder, but this is a rare finding. Urography and ascending pyelography, as well as computer tomography scans are useful in tumor diagnosis. Renal biopsy is seldom indicated because patients usually present when the kidneys are already atrophied.