Pathogenesis and the Management of Renal Failure (Kidney Failure)

The pathophysiologic of CRD involves initiating mechanism specific to the underlying etiology as well as a set of progressive mechanisms that are a common consequence following long-term reduction of renal mass, irrespective of etiology.

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Such reduction of renal mass causes structural and functional hypertrophy of surviving nephrons. Vasoactive molecules mediate this compensatory hypertrophy.

Cytokines, and growth factors and is due initially to adaptive hyperfiltration, in turn mediated by increase in glomerular capillary pressure and flow.

Eventually, these short-term adaptations prove maladaptive, in that they predispose to sclerosis of the rennin-angiotensin axis appears to contribute both to the initial adaptive hyperfiltration and to the subsequent maladaptive hypertrophy and sclerosis.

The definition of CRD requires that the pathophysiologic process described above last more than 3 months. A recently widely accepted international classification divides CRD into a number of stages defined by clinical estimation of the glomerular filtration rate.

These stages help guide clinical diagnostic and management approaches. First, it is important to identify factors that increase the risk for CRD, even in individuals with normal GFR.

Such factors include family history of heritable renal disease, hypertension, diabetes, autoimmune disease, older age, past episode of acute renal failure, and current evidence of kidney damage with normal or even increased GFR.

Such evidence of kidney damage in the face of normal or increased GFR places affected individuals into stage 1 CRD and includes proteinuria, abnormal urinary sediment, or urinary tract structural abnormalities evident on imaging studies.

Even at this stage, when baseline GFR is normal, there is often a characteristic loss of renal reserve. This early stage is particularly well documented in diabetic nephropathy.

Further stage in the pathogenesis of CRD are characterized by a progressive decline in estimated GFR with mild, moderate, and severe stage defined at GFR levels of 60 to 89, 30 to 59, and 15 to 29, respectively.

At a GFR < 15 mL\min per 1.73m sq. , renal replacement therapy may be indicated if uremia is present. For purposes of staging CRD, current guidelines recommend estimating GFR using one of the two equations.

Based on measured plasma creatinine concentration, age, gender and ethnic origin. The normal annual mean decline in GFR with age beginning at age 20 to 30 years is 1mL\per 1.73m sq., reaching a mean value in males of 70 at age 70.

GFR is slightly lower is women than men. By the time plasma creatinine concentration is even mildly elevated, substantial chronic nephrons injury has already occurred.

Albuminuria serves as a key adjunctive tool for monitoring nephrons injury and response to therapy in many forms of CRD. Current guidelines recommend use of albumin-specific dipstick measurement or quantitation by measurement of albumin-to-creatinine ration in a spot first morning urine sample.

Persistence of >17 mg of creatinine in adult females usually signifies chronic renal damage, irrespective of GFR, and can be followed in monitoring natural history and response to therapy, especially in CRD consequent to diabetes, hypertension, or glomerulonephritis.

During stage 1 and 2 CRD, patients after remain free of symptoms, other than that might accompany the underlying etiologic process causing renal disease.

As the decline in GFR progresses to stages 3 and 4, clinical and laboratory complications of CRD become progressively more prominent, virtually all organ systems are affected, but the most evident complications include anemia and loss of energy.

Decreasing appetite and disturbances in nutritional status; abnormalities in calcium and phosphorus metabolism accompanied by metabolic bone disease; and abnormalities in sodium, water, potassium, and acid-base homeostasis.

When GFR falls to <15 mL\min per 1.73 m sq., patients usually experience a severe disturbance in their activities of daily living, sense of well-being, nutritional status, and water and electrolyte homeostasis,

Even-tuating in an overtly uremic state wherein continued survival without renal replacement therapy becomes impossible. The underlying cause of renal disease should be treated aggressively where even possible.

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Blood pressure control

Blood pressure should be reduced to 130\80 mmHg or lower if the patient can tolerate this level of pressure. Adequate control may require a combination of drugs together with large doses of diuretics of contraindications; initial regimens should consist of or include an ACE inhibitor.

Measurement of 24-hour ambulatory blood pressure provides a much more accurate guide to blood pressure control than occasional outpatient clinic recordings.

The aim of management is to prevent or reverse left ventricular hypertrophy, which will itself be significantly underdiagnosed if reliance is placed only upon clinical examination and electrocardiography. Echocardiography is essential.

Hyperkalaemia

Hyperkalaemia often responds to dietary restriction of potassium intake. Drugs, which cause potassium retention, should be stopped. Occasionally it may be necessary to prescribe ion-exchange resins to remove potassium in the gastrointestinal tract. Emergency treatment of severe hyperkalaemia is described.

Acidosis

Correction of acidosis helps to correct hyperkalaemia in chronic renal failure, and may also decrease muscle catabolism. Sodium bicarbonate supplements are often effective, but may cause oedema and hypertension owing to extracellular fluid expansion. Calcium carbonate, also used as a calcium supplement and phosphate binder, has a beneficial effect on acidosis.

Calcium and phosphate

Hypocalcaemia and hyperphosphataemia should be treated aggressively, preferably with regular measurements of serum PTH to assess how effectively hyperparathyroidism is being suppressed. Recent studies indicate that most current assays for PTH also measure a fragment of the molecule that actually inhibits PTH action.

Renal physicians have long recognized that suppression of PTH level to below two or three times the upper limit of ‘ mormal’ carries a high risk of development of adynamic bone disease. This is the probable explanation.

Dietary restriction of phosephate is seldom effective alone, because so many foods contain it. Oral calcium carbonate acts as a calcium supplement and also reduces bioavailability of dietary phosphate.

Aluminum-containing gut phosphate binders have the disadvantage that absorption of aluminum poses the risk of aluminum bone disease and development of cognitive impairment. Recently, the polymer sevelamer has been introduced as a gut-phosphate binder and shows considerable promise.

Treatment with calcitriol or a vitamin D analogue such as alfacalcidol in early renal impairments has no deleterious effect upon renal function provided hypocalcaemia is avoided.

Treatment should probably not development of adynamic bone disease. Vitamin D therapy has the disadvantage that it increases gut phosphate phataemia. Hydrogen antagonists decrease the effectiveness of phosphate binders.

Dietary restrictions

In advanced renal disease, reduction of protein intake lessens the amount of nitrogenous waste products generated, and this may delay the onset of symptomatic uraemia.

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