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Chronic Renal Failure

  • Chronic Renal Failure refers to a slow, progressive reduction in Glomerular Filtration Rate (GFR) and renal function. While it can be precipitated by a variety of etiologies, the basic pathogenic sequence leading to progressive decline in renal function occurs by a common mechanism. If unchecked, the clinical picture of chronic renal failure will ultimately evolve into uremia.
  • Overview
    • Regardless of the precipitating injury, a common pathogenic sequence results in the progressive decline in renal function observed in chronic renal failure. It is a classic story of a initial insult activating mechanisms designed to compensate for the loss of functionality but that in the end become maladaptive.
  • Initial Insult
    • Initial insults which precipitate chronic renal failure cause dysfunction of a subset of glomerulo-nephronic units which eliminates their capacity to successfully participate in filtration. To maintain total GFR, the remaining functional nephrons must compensate for this loss.
  • Compensation
    • Compensation is achieved through hypertrophy and hyperfiltration in the remaining glomeruli and is able to maintain total GFR at acceptable levels for a long time. However, long-term glomerular hyperfiltration results in a set of glomerular morphological changes discussed in compensatory glomerulopathy.
  • Decompensation
    • Eventually the morphological changes associated with compensatory glomerulopathy result in progressive dropout of the compensating glomeruli and their associated nephrons. With the death of each additional glomerulo-nephronic unit, more functional demand is placed on the remaining units to maintain GFR, causing their further hypertrophy and hyperfiltration. Naturally, this accelerates their dropout and ultimately GFR cannot be maintained and undergoes a slow, inexorable decline.
Clinical Consequences
  • Asymptomatic Stage
    • Because of the impressive functional reserve of the kidney early chronic renal failure is largely asymptomatic and may be determined only be nuanced laboratory findings such as increased plasma creatinine. However, clinical symptoms associated with the initial insult, such as diabetic or hypertensive nephropathy, may be apparent.
  • Laboratory Stage
    • As functional units are progressively eliminated a variety of laboratory findings associated with reduced renal resorptive and secretory capacity will become apparent. These will largely be observed with blood chemistries although mild clinical symptoms may also be apparent. These include: Azotemia, hyperkalemia, metabolic acidosis, and hyperphosphatemia.
  • Clinical Stage:
    • Eventually, loss of renal function results in a complete inability to regulate plasma electrolytes, acid-base status, and extracellular volume. In addition, renal secretory capacity of metabolic byproducts along with synthesis of erythropoietin, critical for erythropoiesis, may become compromised. Together, these defects in renal function may manifest as generalized edema, normocytic anemia, oliguria, secondary hypertension, and secondary hyperparathyroidism. Ultimately, in the face of nearly absent renal function uremia will occur (See page).