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Clinical significance of Renal Failure

Updated on November 11, 2011

Acute renal failure lectures

Click on the video and go to Youtube for the Parts 3, 4 and 5


Urological sub-department of the surgical department of Ternopil State Medical University- Ternopil, Ukraine..
Urological sub-department of the surgical department of Ternopil State Medical University- Ternopil, Ukraine.. | Source
The greatest Mukite!
The greatest Mukite! | Source

Renal failure is toxicosis of the body caused by renal dysfunction (self-poisoning). uraemia is a severe form of renal failure. Renal failure and-uraemia occur in acute and chronic cases. Acute uraemia develops in poisoning with nephrotoxic substances (compounds of mercury and lead, carbon tetrachloride, barbiturates, etc, which are very harmful to the Kidney), in transfusion of incompatible blood, profuse haemolysis (break down of red blood cells), and shock. Chronic uraemia develops in the final stage of many chronic renal diseases, such as chronic glomerulonephritis, pyelonephritis, amyloidosis, affections of the renal vessels, tumours of the kidneys, etc.

 It consists in profound homeostatic disorders. It has been established that products of protein decomposition are accumulated in the blood of patients with uraemia. These are nitrogenous slags, such as urea, uric acid, creatinine, and other guanidiries. The content of indican, phenol and other aromatic substances that are formed in the intestine and pass into the blood through the intestinal wall (normally, these substances are eliminated from the blood by the kidneys) increases. Various compounds of sulphur, phosphorus, magnesium, and other substances are accumulated; the ionic equilibrium is upset. Acidosis develops as a result of the accumulation of acid products and disordered production by the kidneys of ammonia that neutralizes the acids. Uraemia is attended by a grave affection of the liver and metabolic disorders.

Acute renal failure and acute uraemia develop due mainly to shock and the accompanying circulatory disorder (mostly in the kidneys). Anoxia develops to cause dystrophic changes in the renal glomeruli and tubules. In I other cases, when acute renal failure is due to poisoning or a grave in I tious disease, its pathogenesis is largely determined by the direct actioi I poisons and toxins on the renal parenchyma. In both cases glomer I filtration is deranged, diuresis decreases and oliguria develops; in se I cases anuria may occur. Salts of potassium, sodium, phosphorus, nit I     products and some other substances are retained in the body.

Acute renal failure rapidly develops and the patient's cond I becomes grave: vomiting, mental confusion, deranged respiration upset heart activity are observed. The glomeruli are affected by ischa to raise the arterial pressure; oedema develops in anuria. The patient die unless anuria and azotaemia are removed during the first few da; the course of the disease is benign, diuresis increases but the concentr ^capacity of the kidneys remains impaired for some time; the renal fun gradually normalizes and the patient recovers.

Clinical picture. Acute renal failure varies slightly, depending o  character of the main disease. In many cases it proceeds with some gesymptoms which make a syndrome. Four stages of acute renal failui distinguished: (1) initial stage lasting from several hours to 6-7 da] clinical picture is characterized by the main symptoms of the di (traumatic or transfusion shock, severe infectious disease, poisoning, _ (2)oligoanuric stage characterized by changes in diuresis (to con / anuria), uraemic toxicosis, and water-electrolyte disorders. Protehcylindruria, and erythrocyturia are revealed on examination, oligoanuric stage can end with death of the patient or his recovery. 1 latter case, diuresis suddenly or gradually increases (the third or poi stage). The specific gravity of the urine is low, the concentrate residual products of protein metabolism in the blood decreases, \ electrolyte balance is restored and the pathological changes in the disappear. The fourth stage, recovery, begins with normalizatic diuresis; it lasts from 3 to 12 months.

Development of chronic renal failure is determined by the progr affection of the kidney parenchyma. The latent period of chronic failure, when renal dysfunction has no clinical symptoms and can oi revealed by special laboratory methods, and the manifested pi characterized by the marked clinical picture of uraemia, are distirgui The latent period can only be revealed by special tests carried oi concentrating capacity of the kidneys and cold food and by the Zimi test. The patient's urine is usually of low specific gravity (below 1 Variations in specific gravity are only insignificant (isohyposthenuria^ clearance tests reveal disordered reabsorption in the renal tubules a glomerular filtration. Mild renal dysfunction can be reveale radioisotope nephrography. It is believed that the first signs of renal f ents with chronic renal diseases only appear when the functioning :hyma diminishes to at least one fourth of its normal size. jgressive renal failure is attended by changes in the circadian varia-n urination: isuria or nycturia are observed. The concentration and >n tests reveal significant disorders in the concentrating capacity of Ineys, pronounced isohyposthenuria (the specific gravity of all urine lens varies from 1.009 to 1.011, i.e approaches the specific gravity of a ultrafiltrate, the "primary" urine). More pronounced disorders in jrption and glomerular filtration are determined by the clearance ind nephrography. Concentration of nitrogenous substances in the gradually increases. Residual nitrogen increases several times (its al content is 14.2-28.5 mmol/1 or 20-40 mg/100 ml). Laboratory :s reveal increased concentration in the blood of various products of in decomposition: urea (3.23—6.46 mmol/1 in norm and 10-15 and times higher in renal failure), creatinine (0.088-0.176 mmol/1 in and 1-1.3 mmol/1 in renal failure), indican (0.68-5.44/xmol/1 in i). It should be noted that the increased blood indican content is often irst and the most reliable sign of chronic renal failure, because its i content does not depend on the protein concentration of food and use it is not accumulated in tissues.

loderately increased concentration of products of nitrogenous decom-/ ion in the blood (azotaemia) may have no effect on the subjective-dtion of the patient for a certain period of time. But later some exter-;hanges become manifest and they can be used for the diagnosis of mia. Certain symptoms of uraemia depend on partial compensation of 1 failure by a more active involvement of the skin, mucosa, and the stive glands in the excretory processes. Decomposition of the urea (ex-:d by the mucosa of the air ways and the mouth) to ammonia by the eria accounts for the specific uraemic breath. In serious cases, the :mic breath can be felt by the physician as he approaches the patient's . It is believed that the uraemic breath can be felt when the concentra-i  of residual  nitrogen  in the  blood  exceeds 70 mmol/1  (about mg/100 ml).

The nitrogenous substances, and in the first instance urea, are liberated :he gastric mucosa and decomposed to form ammonia salts. These salts tate the mucosa of the stomach and the intestine to stimulate nausea, niting (uraemic gastritis), and diarrhoea (uraemic colitis). Irritation of respiratory mucosa causes laryngitis, tracheitis, and bronchitis. Severe matogingivitis develops. The mucosa becomes affected by ulcers and :rosis. Urea crystals (as a white powder) can sometimes be seen on the ient's skin. This is especially noticeable at the orifices of the sweat nds (at the base of hairs). Strong itching develops and the patient scratches his skin. Poisons accumulated in the blood are also liberated by the serous membranes. Uraemic pericarditis is especially characteristic. It can be revealed by auscultating the heart using a stethoscope: the specific coarse pericardial friction can be heard. This friction appears in the terminal period and is a sign of  approaching death.

Memory and sleep become deranged due to general poisoning; weakness, dull headache, somnolence, apathy and deranged vision arecharacteristic. Examination of the fundus oculi reveals narrowed arteries and dilated veins, oedema of the papilla of the optic nerve, and whitish local foci (retinopathy). Development of retinopathy is explained by trophic disturbances due to The vascular spasm of the fundus oculi vessels and uraemic toxicosis which intensifies these changes. The pupils are usually narrowed.

Metabolic disorders are pronounced: the patient develops cachexia; the liver and bone marrow functions are affected by dystrophy; toxic uraemic anaemia develops which is usually attended by leucocytosis and thrombocytopenia. The tendency to haemorrhages develops due to a decreased blood platelet count, disorders in the blood coagulating system and in creased capillary permeability (as a result of toxicosis). Haemorrhages of the gastro-intestinal tract, urinary tract, uterus, and the nose may develop. Skin haemorrhages also occur. The body temperature slightly decreases.

Later, toxicosis increases, the patient's consciousness becomes dimm ed, and uraemic coma develops. Periods of stupor alternate with periods of excitation, hallucinations, and noisy slow breathing with very deep inspira- tions (Kussmaul's breathing); respiration with alternating periods of hyperpnoea and apnoea (Cheyne-Stokes respiration) occurs less frequently. At the terminal stage the patient is in a deep coma; muscular twitchings occur at times and the patient dies.

There is no universally accepted classification of chronic renal failure at the present time. Three stages are usually differentiated: (1) the initial stage with insignificantly increased residual nitrogen and creatinine and moderately decreased glomerular filtration; (2) pronounced stages (IIA and IIB) with marked azotaemia and electrolyte disorders and (3) terminal stage with a pronounced clinical picture of uraemia.

Main principles of treatment. Patients with acute renal failure should be immediately taken to hospital. Treatment should be begun as early as possible and aimed at eliminating the main aetiological factors (removal of nephrotoxic substances or their detoxication, giving large doses of plasma or blood substitutes for hypovolaemic shock). The electrolyte equilibrium should be corrected simultaneously. Mannitol or furocemid should be given intravenously in the initial functional stage of acute renal failure to restore diuresis. Haemodialysis (artificial kidney) or peritoneal dialysis are necessary in grave cases.

The protein content of the diet is controlled in patients with chronic renal failure. Therapeutic action on the aetiological factor and pathogenic mechanisms should be attempted (antibacterial therapy in pyelonephritis, immunodepressants in chronic glomerulonephritis, etc.). The water-electrolyte equilibrium and acid-base balance are corrected simultaneously. The necessary symptomatic therapy with hypotensive, cardiovascular and other preparations should be carried out. In severe cases, permanent chronic haemodialysis is carried out or the kidneys are transplanted to prolong the patient's life.


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    • D.Virtual.Doctor profile imageAUTHOR

      Funom Theophilus Makama 

      6 years ago from Europe

      thanks a lot

    • D.Virtual.Doctor profile imageAUTHOR

      Funom Theophilus Makama 

      7 years ago from Europe

      you guys are great..

      Thanks a lot

    • profile image


      7 years ago

      hi D.V.D

      hi al_masculine, it seems we are in a kind of a competition on who comments first on our honorable Doctor's hubs.... I promise to beat you next time.

      Great job D.V.D

    • profile image


      7 years ago

      wow! Those videos have been of good help to me. Above all, this is good. Renal failure is very common nowadays... I will do more research on its prevalence rate and statistics... Good work D.V.D


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