Outline of the treatments of chronic kidney disease
Histology of acute glomerulonephritis
Clinical approach to the patient with chronic kidney disease
You have to find answers to following questions when you approach to the patient.
1. Is there any life threatening complication of chronic kidney disease (CKD)?
2. Does the patient have chronic renal failure?
3. Are there factors , operating which have caused or are causing acute reduction in chronically impaired renal function? ?
4. What is the cause of CKD?
5. What measures are needed to delay progression?
6. Are there complications of CKD that require specific treatment?
(1) Is there any life threatening complication of CKD?
Before go into anything you have to correct any life threatening conditions that patient has.
- Metabolic acidosis
- Pulmonary edema
- Severe anemia
(2) Does the patient have chronic renal failure?
- History of more than 6 months of ill health, long standing hypertension, proteinuria, nocturia for more than 6 months.
- Pallor, pigmentation, pruritus, brown nails, evidence of long standing hypertension.
- Normochromic anaemia , small kidneys on ultrasound ( except : diabetes , amyloid , myeloma , adult polycystic kidney disease ), renal osteodystrophy on radiography.
(3) Are there factors, operating which have caused or are causing acute reduction in chronically impaired renal function?
- Dehydration from diarrhea, diuretics, surgery
- Cardiac failure
- Pericardial tamponade
- Renal vascular disease
- Drugs, especially ACE inhibitors + NSAIDS
- Systemic infection
Obstruction and infection of the urinary tract
- Papillary necrosis and sloughing
- Bladder cancer
- Polycystic cysts
Metabolic and toxic
- Contrast media
Progression of underlying diseases
- Relapse of nephritis.
- Development of accelerated phase of hypertension.
- Renal vein thrombosis usually in chronically nephrotic patients.
(4) What is the cause of CKD?
- Polycystic kidney
(5) What measures are needed to delay progression of CKD?
- Dietary restriction of protein
- Treatment of Hypertension
- Good glycemic control in patients with diabetes mellitus
- Treatment of hyperlipidemia
- Avoidance of nephrotoxic drugs
Dietary restriction of protein
Dietary manipulation (low-protein diet) has long been advocated as a means of retarding CRF
Treatment of hypertension
- Diuretics - Loop diuretics are more effective.
- ACE inhibitors - Effective, Specially in diabetes mellitus (May decrease GFR in advanced CRF, renal artery disease).
- Calcium channel blockers - Reduce proteinuria?. Non - Dihydropyridine ones are preffered.
Treatment of underlying disease
- If the CKD is due to diabetes mellitus, good glycemic control retards the progression of CKD.
- Treatment of hyperlipidemia to target levels.
- Avoidance of nephrotoxins - IV radiocontrast, nonsteroidal anti-inflammatory agents, aminoglycosides.
(6) Are there complications of CRF that require specific treatment?
- Prevention of progressive changes in the arteries and heart associated with uremia may be possible by correction of recognized cardiovascular risk factors.
Currently accepted strategies
- Cessation of smoking and other healthy lifestyle modifications.
- Treatment of hypertension.
- Treatment of lipid abnormalities.
- Treatment of anemia.
- Tight glycaemic control in patients with diabetes.
- Control of plasma calcium and phosphate levels.
- Management of hyperparathyroidism.
- Management of renal anemia is based on administration of erythropoietin with iron therapy.
- Current recommendations suggest that erythropoietin therapy should be commenced once the hemoglobin concentration declines below 10 g/dl and the recommended target hemoglobin concentration in dialysis patients is about 11–12 g/dl.
- The drug is best given subcutaneously.
- The usual starting dose is about 2000 units two or three times per week; Ideally hemoglobin level should rise by 1 g / dl per month.
- A reticulocyte response is obtained within 3–4 days of starting treatment, and the hemoglobin concentration usually begins to increase from 2 weeks onwards.
Benefits of Erythropoietin therapy
- Amelioration of the symptoms of anemia.
- Reduction of high cardiac output.
- Increased peripheral vascular resistance.
- Improvement in myocardial ischemia.
- Reduced left ventricular mass.
- The mainstay of prevention and treatment of renal osteodystrophy is the maintenance of normal blood divalent ion concentration (particularly phosphorus).
- Biochemical and radiological monitoring is essential.
- It is best to start treatment early, when creatinine clearance declines to about 40 ml/minute.
- At this stage, dietary reduction of phosphate with an adequate calcium intake may be effective.
- Calcium carbonate or calcium acetate, 2–8 g/day, is currently the binder of choice.
- Sevelamer hydrochloride (RenaGel – a non-absorbable polymeric phosphate binder) is a promising new agent ( It is calcium-free and binds phosphate through ion exchange and hydrogen binding).
Suppression of PTH
- Treatment with oral calcitriol can be titrated according to PTH levels; the dose usually ranges from 0.25 µg on alternate days to 1 µg/day.
- Combined use of calcium salts and calcitriol increases the risk of hypercalcemia, and regular blood monitoring is therefore required.
- Pruritus is the most exasperating symptom.
- A number of explanations are advanced including sensitivity to histamines, a raised calcium phosphate product, and uremia itself.
- Treatment includes starting or increasing dialysis, applying skin emollients, controlling the plasma phosphate level, keeping cool, and the prescription of antihistamines, for example chlorphenamine (chlorpheniramine) 4 mg at night (which is also slightly sedative).
- Naltrexone, an opioid antagonist, and ultraviolet phototherapy are effective in the short-term.