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Tubule dealt from functional and anatomic location in the proximal tubule, Loop of Henle, distal tubule and collecting pipes. The blood is filtered in glomeruli and the filtrate changed the way through tubule by absorption of substances to be returned to the blood and secretion of substances to be excreted by the body.

Interstitial tissue surrounding the nephrons and consists of interstitial cells (fibroblasts and lymfocyttlignende mononuclear cells) and extracellular matrix. In a normal kidney would amount interstitial tissue being sparingly and glomeruli and tubules are close together without visible interstitium between. The amount interstitium normally increase in medullary areas. The production of erythropoietin occurs in interstitial cells. Otherwise binds interstitiet Nefron together and are part of the body's immune system.

Disease processes affecting tubules and interstitium collected. Interstitial inflammation will damage tubulusceller and affect tubular function, while the tubular damage may cause interstitial inflammation. We treat these diseases therefore collected as tubulo-interstitial diseases. Primary disease processes in tubules will affect the function and structure of the glomeruli in the same manner as glomerular diseases leading to secondary tubulo-interstitial changes. In a chronic end stage renal disease will all be present glomerulosclerosis, interstitial fibrosis and tubulusatrofi. The patient gets contracted kidney and the original disease process can no longer be identified.

It is useful to divide tubulo-interstitial diseases in acute and chronic. The acute has inflammatory character and termed tubulo-interstitial nephritis, while the chronic steeped tubulusatrofi and interstitial fibrosis, with less inflammation and is often described as tubulo-interstitial nephropathies. Various infections and medications are frequent causes of both acute and chronic disease processes. In addition, toxins, systemic conditions and genetic defects may lead to chronic tubulointerstitial nephropathy.

Polyuria, acidosis and electrolyte disturbances may be signs and symptoms of disturbed tubulusfunksjonen. Genetic defects or disease processes tubulointersitielt can affect urine composition and renal konsentreringsevne and thus contribute to tubulointerstitial disease can be detected before glomerular filtration rate is affected and the patient develops renal impairment.