Renal diseases

Forth stage

Medicine
Lecture-4
د.عماد البدراني

31/10/2015

Chronic Renal failure

Definition:

Is an irreversible deterioration in renal function which classically develops over period of years . Initially manifested only as biochemical abnormality, eventually loss of excretory, metabolic, and endocrine function of the kidney lead to development of clinical symptoms and signs of renal failure which is referred to as uremia
Etiology
Pre-renal
Include long standing R.A.S
2) Renal causes
Include chronic G.N chronic interstitial nephritis, D.M hypertension, C.T disease (S.L.E) myeloma, amyloidosis, radiation nephritis, and neoplasia
3) Post-renal causes
Due to long standing urinary obstruction


Pathogenesis:
Disturbances in water, electrolytes and acid-base balance, contribute to clinical picture in patient with chronic renal failure but the exact pathogenesis of clinical syndrome of uremia is unknown. And many substances present in abnormal concentration in the plasma have been suspected of beinguremic toxins
Clinical feature
In early CRF the patient is often asymptomatic,
Renal failure may present as raised urea and creatinine found during routine examination, often accompanied by H.T proteinuria or anemia
Symptoms usually develop when G.F.R reach 20ml/min.And nocturia
(Due loss of concentration ability and osmotic load).
Is often early symptoms and then because of wide spread effect of renal failure, symptoms and signs develop related to almost every body system.

1-Anemia : anemia is common and usually correlate with the severity of CRF and contribute to many of the non-specific symptoms of CRF.
Causes:
relative deficiency of erythropoietin
diminishederythropoiesis due to the toxic effects of uremia on bone marrow
reduced red cell survival
increased blood loss due to capillary fragility and poor platelet function
reduced dietary intake and absorption of iron and other hematocrits

They found in the cystic disease of kidney the anemia is rare,while in the interstitial nephritis the anemia is so sever.
Anemia can be treated by synthetic human erythropoietin {Eprex} and it is effective in treat anemia. Butit cause side effect like tingling sensation and S.T convulsion and lead to uncontrolled hypertension, failure of erythropoietin therapy is due to iron deficiency or active inflammation or malignancy or aluminum over load
2-Renal- osteo dystrophy:
The metabolic bone disease accompanied CRF consist of admixture of:
Osteomalcica: (due to decrease activity od 1-alph hydroxylase enzyme of vit. D) which lead to decrease intestinal absorption of calcium and lead to hypocalcaemia and reduce calcification of osteoid
Oestitis fibrosis: Cystic decalcified lesion in bone due to secondary hyper parathyroidwhich is stimulated by low plasma calcium and by hypophosphatemia. In some patient tertiary or autonomous hyper parathyroid with hypocalcaemia develops
Osteoporosis: occur in many patient possibly related to malnutrition
Osteosclerosis: is seen mainly in the sacral area at the base of the skull
And in the vertebrae, the cause is unknown.
3- Myopathy:
Generalized myopathy is due to:
A) Poor nutrition
b) Hyperthyroidism
c) Vit. D deficiency
d) Electrolyte disturbances


Muscle cramps is common can be treated by quinine sulphate
restless leg patient legs are jumpy during night maybe trouble treated by clonazepam

4-Neuropathy:

There is demyelination of modulated fiberLead to:
Sensory neuropathy present as parenthesis
Motor neuropathy present as foot drop
Autonomic neuropathy present as delayed gastric empty, diarrhea ,postural hypotension
The clinical manifestations of neuropathy appear late in in curse of CRF

5- Endocrine function:

Number of hormonal abnormities may be present like:
Hyperprolactinemia
Hyperparathyroid
In femaleamenorrhea is common
In both sexes there is loss of libido and sexual function
Half-life of insulin is prolonged.
6-Cardiocascular disease:
hypertension develops in 80% of patient with CRF due to Na retention, increase rennin and increase aldosterone ( hypertension should be well controlled )
atherosclerosis is common and may be accelerated by hypertension
vascular calcification may develops
pericarditis is common in untreated or inadequate Rx and it may lead to pericardial tamponade and late constructive pericarditis


7-Acidosis : due to decline renal function and this acidosis usually asymptomatic and lead to proton buffered in bone in place of calcium, this aggravating metabolic bone disease
8-infection: cellular and humoral immunity are impaired with increased susceptibility to infection ( infection is the most common cause of death in dialysis patients after cardiovascular diseases )
9-GIT disturbance : very common and presented as anorexia, nausea, vomiting and abnormal bowel motion, also CRF patients are vulnerable to gastric and duodenal ulceration

Management of CRF

there are several aspects:
identify the underlying disorder by history, physical examination, biochemical tests, immunology, radiology and renal biopsy ( in some cases the cause may be amenable ti specific therapy e.g. immunosuppression in some types of GN )
search for reversible factors and the correction of which may result in improvement in renal function, like:
hypertension
decrease renal perfusion ( renal artery stenosis, decrease BP due to drugs, Na and water depletion, poor cardiac function )
UT obstruction
UTI
other infection
nephrotoxic medication

progression of CRF

a plot of reciprocal serum creatinine concentration against time allows good follow up, when patient need dialysis and detect any worsening of renal function

Factors of progression of CRF

1- control of BP : good control of BP is beneficial especially in disease affecting the glomerulus and may retard deterioration of CRF and diabetic and with heavy proteinemia. ACE-I is more effective in diabetic nephropathy
2-Diet : in experimental studies, progression of renal failure can be retarded by dietary manipulation mostly by restriction of dietary protein.
in human studies results have been less clear cut for most patients living in areas where renal replacement therapy is available severe protein restriction is not generally recommended. moderate restriction (60g/day) should be accompanied by adequate calories to prevent malnutrition. anorexia and muscle loss may indicate a need to start dialysis Rx.
3-lipid : hypercholesterolemia is almost universal in patients with proteinuria and increase Triglyceride level is common is patient with CRF, these accelerate development of vascular diseases and accelerate progression of CRF. should be treated.
4-electrolytes and fluid : in CRF, kidney cannot concentrate urine, so high volume of urine is needed to excrete products of metabolism and fluid intake of 3 liters per day is desirable, some patients with "salt-wasting" may require high sodium and water intake ( these seen in patient with cystic diseases, obstruction,reflux nephropathy and other tubulointerstitial diseases but not seen in glomerular diseases ), limitation of potassium intake to 70mmol/day is required
5-Osteodystrophy:
plasma calcium and phosphate should be kept as near to normal as possible, hypocalcaemia is controlled by giving 1-alpha-Vit D ( synthetic analogue of Vit D )
hyperphosphatemia is controlled by dietary restriction of food with high phosphate content as milk ,cheese and eggs. use of phosphate-binding drugs as calcium carbonate tablet 500mg 1*3, aluminum OH is also a phosphate binder 300-600 mg before meal, side effects are constipation and aluminum toxicity
hyperparathyroidism is controlled with these measures, rarely the patient needs parathyroidectomy


Renal replacement therapy in CRF
Haemodialysis : should be started when despite adequate medical Rx, the patient with advanced renal failure and before developing serious complication, this occur when serum creatinine 800 mircomol (9mg). vascular access is needed and in emergency state a central venous catheter is needed. hemodialysis is for 3-5 hours 3times/week
CAPD "Continuous Ambulatory Peritoneal Dialysis"
Renal transplantation