RENAL DISEASE

Pathological polyuria observed in various pathological conditions , can be short or long .
Short-term pathological polyuria observed after some attacks, which are based on vasomotor disturbances , for example, after an attack of angina , migraine and others to advance in these cases after a single bout of excessive excretion of urine associated with changes in the circulation of the glomeruli of neurogenic origin .
With the convergence of edema, which most often occurs under the influence of diuretics , also takes short polyuria . Of some diuretics cause increased filtration resulting in improved glomerular circulation ( eg , digitalis ) , others suppress reabsorbtsionnuyu function of tubular epithelium ( novurit ) .
Short-term polyuria also observed with resorption transudate and exudate accumulated in body cavities , and even celebrated in the first 3-4 days after recovery from acute infectious diseases.
Prolonged pathological polyuria is usually observed when diabetes insipidus (diabetes insipidus). In this disease, the pathology observed in maximum numbers of daily urine output, which may reach 20-25 liters. Such a large polyuria accompanied by a sharp polydipsia ( increased thirst ) . Cause of polyuria in this disease associated with pituitary lesion , consider loss of antidiuretic hormone action , which , as mentioned above , stimulates tubular reabsorption . Diabetes insipidus can also occur when certain lesions of the midbrain , which is the pituitary gland in close functional relationship .
In diabetes daily diuresis can reach 8-10 l, rarely more . Cause of polyuria in diabetes is high osmotic pressure of glucose in the urine provisionally preventing water reabsorption tubular epithelium . In addition , there is a direct and lowering functions reabsorbtsionnoy tubular epithelium .
When malnutrition polyuria can often be observed along with the swelling . When the disease reaches daily diuresis 3-5 liters . Reason polyuria when malnutrition is not completely clear . It must be assumed that its mechanism play a role : 1) copious amounts of fluid consumed often such patients , 2 ) lowering the production of antidiuretic hormone by the pituitary gland , and 3) an increase in glomerular filtration due to the decrease kolloidoosmoticheskogo plasma pressure due to hypoproteinemia ( percent decrease in plasma proteins ) .
As for kidney disease , it is a symptom of polyuria far-gone chronic glomerulonephritis and the so-called malignant nephrosclerosis . The amount of urine reaches in these diseases 3-5 liters per day , rarely more . The released urine pale, watery and has a low specific gravity.
The mechanism of polyuria in chronic glomerulonephritis and malignant nephrosclerosis associated with these diseases in developing kidney shrinkage . Thus as a result of glomerular capillaries and zapustevaniya growths on their site scar connective tissue progressively reduced the number of functioning glomeruli. The result is a gradual decrease in kidney filtration surface , and therefore , a provisional dip daily amount of urine. Since the blood supply of tubular epithelium , and hence its function is dependent on the preservation of blood flow in the respective glomeruli , then at least the last zapustevaniya worsens blood flow tubular epithelium . Thus, the parallel decrease in glomerular filtration and tubular reabsorption falls . Calculations show that even in a strong fall filtration slight decrease reabsorption is already enough to significantly increase the amount of urine . Therefore, polyuria with shrunken kidneys is the result of a sharp drop in tubular reabsorption . This polyuria can occur even when limiting the amount of fluid drunk patients . Hence its name : "forced polyuria ."
With further renal atrophy number of functioning glomeruli become so small and so falls filtering that despite further decrease the amount of the final reabsorption of urine is below normal . Then polyuria replaced oliguria . Rapid decrease in glomerular filtration rate and thus contributes to the fall performance of the left ventricle as a result of these diseases peculiar to prolonged hypertension. Weakening of the left ventricle leads to reduced blood flow in a few surviving glomeruli , leading to further reduction filtering.
" Forced polyuria " due to shrinkage of the kidneys can also be observed in the final stages of renal amyloidosis and cystic degeneration of them .
With regard to surgical diseases of the kidneys and urinary organs diseases , the temporary or prolonged polyuria frequently observed in chronic pyelonephritis , prostatic hypertrophy , renal tuberculosis , etc. This is sometimes the result polyuria reflex changes of the glomerular circulation, but more often the cause of polyuria and in these diseases processes are wrinkling kidney