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The renal tubule is divided up based on function and anatomy into the proximale convoluted tubule, the loop of Henle, the distale convoluted tubule and the collecting duct.. The blood is filtered in the glomeruli and the filtrate is altered on the way through the renal tubule by absorption of substances back to the blood and secretion of substance that will be excreted from the body.

Interstitial tissue surrounds the nephron and consists of interstitial cells (fibroblasts and lymfocyte-like mononuclear cells) and extracellular matrix. In a normal kidney, the amount of interstitial tissue is sparing and the glomeruli and tubules are packed close together without visible interstitium between. The amount of interstitium normally increases in the medular area. Production of erytropoietin occurs in the interstitial cells. Otherwise, the interstitium binds the nephrons together and is a part of the body's immune defence.

Diseases affect the tubules and the interstitium together. Interstitial inflammations will damage tubule cells and affect tubular function, simultaenously, the tubular damage will lead to interstitial inflammation. Therefore, these diseases are treated together as tubulointerstitial diseases. Primary diseases in the tubule will affect the function and structure of the glomeruli in the same way that glomerular diseases lead to secondary tubulointerstitial changes.Glomerulosclerosis, interstitial fibrosis and atrophy of the tubule. can be found in the chronic end-stage of all kidney diseases. The patient's kidneys shrink and the original disease can no longer be identified.

It is useful to divide tubulointerstitial disease into acute and chronic diseases. The acute are charcterised by inflammation and are called tubulointerstitial nephritis, while the chronic are characterised by atrophy of the tubules and interstitial fibrosis, with less inflammation and are often called tubulointerstitial nephropathies. Different infections and medications are frequent causes of both acute and chronic diseases. In addition, toxins, systemic diseases and genetic defects can also result in chronic tubulointerstitial nephropathy.

Polyuria, acidosis and electrolyte imbalances are possible symptoms and signs of disturbances in the function of the tubule. Genetic defects or diseases of the tubulointerstitium can affect the composition of the urine and the kidneys' ability to concentrate and thereby contribute to identifying tubulointerstitall diseases before the glomerular filtration rate is affected and the patient develops reduced kidney function.