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Chronic Renal Failure

Clinical features, Diagnosis, Management, Prognosis,

Chronic renal failure is irreversible deterioration in renal function. It is characterised by impairment of excretory, metabolic and endocrine functions of the kidney that leads to the development of the clinical syndrome which is referred to as uraemia. Chronic renal failure may be caused by any condition which destroys the normal structure and function of the kidney. In many patients the condition progresses insidiously over a number of years and frequently at presentation it is impossible to determine the underlying renal disease. 

Chronic renal failure can be caused by:

       Diabetes mellitus (the most common cause but it probably takes at least 15 years)

       Long-standing hypertension (very common)

       Vasculitis (small blood vessel disease) in systemic lupus erythematosus (SLE) and systemic sclerosis (scleroderma) caused by deposition of immune complexes in blood vessel walls with subsequent inflammation

       Various types of glomerulonephritis (discussed earlier), many of unknown cause

       Hereditary polycystic kidney disease characterised by many bilateral renal cysts that increase renal size but reduce the volume of functioning renal tissue

       Chronic pyelonephritis, especially associated with chronic vesico-ureteric reflux

       Analgesic nephropathy caused by long-term anti-inflammatory or analgesic treatment (e.g., in rheumatoid arthritis)

       Long-standing urinary stones, especially of staghorn variety

       Unknown causes (idiopathic) 

Pathogenesis of uraemia is not completely understood. Disturbances in water, electrolytes and acid-base balance undoubtedly contribute to the clinical picture but the exact pathogenesis of the clinical syndrome of uraemia is unknown. Almost any substance present in abnormal concentration in the plasma has been suspected of being a ‘uraemic toxin?/i>. It is most likely that the syndrome is caused by accumulation in body fluids of a number of substances among which must be included phosphate, urea, creatinine, guanidine, phenols and indols. There is no satisfactory way of assessing the biological toxicity of different substances but it must be assumed that the uraemic toxins are substances eliminated by the normal kidney and retained in renal failure.

Clinical features:  < BACK TO TOP >

           In the early stages of the disease, the patient may be asymptomatic and the existence of renal insufficiency may be revealed by discovery of proteinuria, anaemia, secondary hypertension or raised blood urea and creatinine during routine examination.

           It is not uncommon for patients to remain asymptomatic until the glomerular filtration rate (measured by the creatinine clearance test) is 22 L/day of less.

           Subsequently, symptoms and signs are referable to almost every system and many patients present with complaints which at first sight may not suggest their renal origin:

                Vague ill-health

                Generalised weakness and lack of energy, muscle aches

                Breathlessness on exertion

                Anorexia, nausea, vomiting and an unpleasant taste in the mouth

    Disordered intestinal motility, usually diarrhoea (direct damage of the gastrointestinal lining as well as possible effect of hyperkalaemia) but sometimes constipation

                Headaches and visual disturbances, due to associated hypertension

    Pallor and pigmentation resulting in characteristic yellow-greyish colour of the skin; some patients report troublesome pruritus (skin itching)

           The rate of progression to end-stage renal failure is very variable.

           Characteristically, the patients are free from oedema despite reduced glomerular filtration, which is probably due to compensatory decrease in sodium and water reabsorption to maintain normal urine volume (there is no oliguria until late stage).

           Acidosis contributes to the dyspnoea and respirations are deep (hyperpnoea), later drowsiness, confusion and coma develop.

           Almost all organs can be affected in some way: 

    1. Anaemia

    This is common and to some extent reflects the severity of uraemia.

    Several factors contribute:

    1. Reduced dietary intake of iron due to anorexia as well as impaired intestinal absorption of iron due to disturbed gastrointestinal motility and mucosal toxic damage

                3. Diminished erythropoiesis due to toxic effects of uraemia on bone marrow cells

                4. Reduced red cell survival again due to toxic effects

    5. Decreased production of erythropoietin (EPO) in the kidneys, the hormone that normally stimulates production of erythrocytes in the bone marrow; this is probably the most important factor 

    2. Renal osteodystrophy

    Metabolic bone disease consists of osteomalacia (soft bones with abundant osteoid but               

         that lack minerals) and osteoporosis (hard but brittle bones due to the loss of whole bone      


    The main problem appears to be failure of the kidney to convert cholecalciferol (vitamin  

         D) to its active metabolite 1,25-dihydroxycholecalciferol (calcitriol) which impairs   

         calcium absorption from the gut. End result is low plasma calcium levels, reduced  

         mineralisation of bone, and subsequent secondary hyperparathyroidism which initiates

         mobilisation of calcium from bones. 

    3. Neuropathy

    Demyelination (loss of myelin sheaths) of fibres causing sensory neuropathy

    (paraesthesiae-tingling, numbness, burning feeling), motor neuropathy (muscle weakness/paralysis such as foot drop) and autonomic neuropathy (disorders of gastro-intestinal motility in form of constipation).

    Symptoms and signs of neuropathy improve when dialysis is started.


    4. Endocrine functions

    Loss of sexual drive in both sexes, amenorrhoea in females, erectile dysfunction in males.

    Uraemia is frequently mistaken for hypothyroidism because both have very similar  


    5. Cardiovascular disorders

    Hypertension in approximately 80% of patients usually related to hypervolaemia and/or  

         activation of the renin-angiotensin-aldosterone system as a result pf reduced glomerular 

        filtration; atherosclerosis is also common.

    Hypertensive and/or ischaemic congestive heart failure may later develop.

    Uraemic toxic pericarditis is common in untreated end-stage renal failure and may    

         present as persistent retrosternal burning or stabbing chest pain that becomes worse on    

         deep breathing or swallowing (irritation/friction on the pericardium). 

    6. Impairment of cellular and humoral immunity with increased susceptibility to infections.

Diagnosis:  < BACK TO TOP >

             Blood analysis shows elevated urea and creatinine, sodium concentrations are usually normal and potassium levels normal to moderately elevated (< 6 mmol/L).

             Creatinine clearance is always reduced, depending on the stage of the disease, reflecting reduced glomerular filtration.

             Hypocalcaemia and hyperphosphataemia are found regularly and reflect deranged calcium metabolism.

             There is usually moderate acidosis and normochromic-normocytic anaemia.

             Findings on urine analysis depend on the nature of the underlying disease.

Management  < BACK TO TOP >

           Initially the following measures are advisable, although they do not address the underlying cause:

    Treatment of hypertension, urinary tract infection, urinary tract obstruction,  

         sodium and water depletion (if present), nephrotoxic drugs should be avoided.

                Control of diet (limit dietary protein if plasma creatinine very high, seen only in

         terminal stage).

    Water and sodium are not restricted unless there is visible oedema, potassium

         intake doesn’t have to be reduced until end-stage renal failure.

    Renal osteodystrophy is treated with calcitriol [Calcijex, Sitriol, Rocalcitrol], a  

         synthetic analogue of vitamin D which doesn’t need activation in the kidney.

    Human recombinant erythropoietin [Eprex] weekly injections are given to 

         improve anaemia. 

           In patients with progressive destruction of renal tissue, there comes a point when supportive measures are required:

    Haemodialysis is started usually with a creatinine in the region of 1,000 mmol/L   

    and is carried out for 4-6 hours 3 times weekly.

    Continuous ambulatory peritoneal dialysis (CAPD) uses the peritoneum as a 

    dialysis membrane. Dialysis fluid (around 1.5-3 L in adults) is introduced into the   

    peritoneal space through a permanent catheter (a tap in the abdominal wall) and periodically drained and replenished 4 times/day by the patient. Peritonitis can develop as a complication.

    Renal transplantation is the most effective treatment, but tissue types must be

    matched as closely as possible and this procedure must be followed by

    immunosuppressive treatment (infections and malignancies are unwanted effects).

Prognosis  < BACK TO TOP >


(source : Dr Zoran Pletikosa)

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