Presentation on theme: "Renal insufficiency Renal insufficiency is a pathological process in which the functions of kidney are severely damaged, leading to the accumulation of."— Presentation transcript:
Renal insufficiency Renal insufficiency is a pathological process in which the functions of kidney are severely damaged, leading to the accumulation of metabolic products, drugs and poisons, and disorders of water, electrolyte, acid- base balance, and renal endocrine function. Renal failure: the terminal stage of renal insufficiency
Renal insufficiency Dysfunction of glomerular filtration Dysfunction of renal tubule Renal endocrine dysfunction
Decreased GFR a decrease in renal blood flow a decrease in glomerular effective filtration pressure a decrease in glomerular capillary surface area a decrease in glomerular filtration coefficient Increased permeability of glomerular filtration membrane Dysfunction of glomerular filtration
Dysfunction of renal tubules Dysfunction of proximal convoluted tubules reabsorbing water, glucose, protein, amino acids, phosphate, bicarbonate, sodium, potassium Dysfunction of Henles’ loop reabsorbing chloride, sodium Dysfunction of distal convoluted tubules and collecting ducts secreting hydrogen, potassium and ammonia
Renal endocrine dysfunction Renin-angiotensin-aldosterone system A decrease in erythropoietin (EPO) 1,25-dihydroxyvitamin D3 Kallikrein-kinin-prostaglandin system Decreased deactivation of parathyroid hormone (PTH) and gastrin
Acute renal failure Acute renal failure represents a rapid decline in renal function leading to increased blood levels of nitrogenous wastes and impaired water and electrolyte balance, and manifesting water intoxication, azotemia, hyperkalemia, and metabolic acidosis.
Acute renal failure is reversible if the cause can be identified and corrected before permanent kidney damage has occurred. The most common indicator is azotemia, which is an accumulation of nitrogenous wastes (urea nitrogen, uric acid and creatinine)
Etiology and classification Prerenal failure Intrarenal failure Postrenal failure
Prerenal failure- functional failure Prerenal failure is the most common form of acute renal failure. It is caused by a marked decrease in renal blood flow. Causes Hypovolemia Heart failure Intrarenal vasoconstriction Increased blood vessel bed
Intrarenal failure- parenchymal renal failure Intrarenal failure results from conditions that can cause damage to structures within the kidney, glomerular, tubular and interstitial.
Causes Acute tubular necrosis (ATN) Prolonged renal ischemia (ischemic ATN) or ischemia-reperfusion injury Toxic insult of tubules by drugs, heavy metals (nephrotoxic ATN) Intratubular obstruction hemoglobin and myoglobin severe hypokalemia, hypercalcemia Acute glomerulonephritis and acute pyelonephritis
Postrenal failure – obstructive renal failure Obstruction of urine outflow from the kidneys. (ureter, bladder and urethra) Prostatic hypertrophy (most common)
Pathogenesis Decreased renal blood volume Renal tubular injury renal tubular obstruction increased intraluminal P back leak of the glomerular filtrate decreased urine; interstitial edema impressing renal tubules and peri-tubular capillaries Renal cell lesion renal tubular cells, endothelial cells and mesangial cells necrotic (tubulorrhexic and nephrotoxic) and apoptotic ATP↓oxygen free radical↑reduced glutathione(GSH) ↓phospholipase ↑ cytoskeletal structural change activation of cell apoptosis
Alterations of metabolism and function The oliguric stage The diuretic stage The recovery stage Oliguric type and nonoliguric type Oliguric type
The oliguric stage Urinous alterations Water intoxication Hyperkalemia Metabolic acidosis Azotemia
Urinous alterations oliguria, anuria hyposthenuria, isosthenuria an increase in urine sodium hematuria, albuminuria, cyclindruria
Water intoxication excretion ↓ (due to decreased GFR) ADH ↑ (due to activation of RAS or decreased ECV) endogenous water from catabolism ↑ water uptake ↑
Hyperkalemia excretion ↓ tissue injury and increased catabolism, acidosis hyponatremia transfusion of storage blood or excessive intake from food or drugs
Metabolic acidosis decreased excretion of acidic metabolites decreased secretion of hydrogen and ammonia increased production of fixed acids
The diuretic stage Restoration of renal perfusion and glomerular filtration Reduced reabsorption function of neonatal renal tubules Release of renal obstrction Osmotic diuretics The recovery stage
Treatment of acute renal failure Identifying and correcting the causes Maintaining water and electrolyte balance Supplying adequate calories Dialysis
Chronic renal failure Chronic renal failure represents progressive and irreversible destruction of kidney structures, leading to the accumulation of metabolic products, drugs and poisons, and disorders of water, electrolyte, acid-base balance, and renal endocrine function. Diabetes Hypertension Glomerulonephritis
Stages of progression Chronic renal failure is characterized by a reduction in the number of functional nephrons. The rate of nephron destruction ranges from several months to many years. Diminished renal conserve Renal insufficiency Renal failure Uremia
Pathogenesis Several hypothesis on chronic failure Intact nephron hypothesis Trade-off hypothesis Glomerular hyperfiltration hypothesis
Mechanism of nephron dysfunction Actions of primary disease Secondary and progressive glomerular sclerosis protein flux local inflammation glomerular DIC Tubulointerstitial injury
Alterations of function and metabolism Alterations of urine Azotemia Disorders of water, electrolyte and acid-base balance Renal hypertension Renal anemia Tendency to hemorrhage Renal osteodystrophy
Alterations of urine Early stage polyuria, nocturia, isosthenuria, protein, RBC, WBC in urine Late stage oliguria
Disorders of water, electrolyte and acid-base balance Edema or dehydration Salt-wasting Hypokalemia (early) or Hyperkalemia (late) Hyperphosphatemia Hypocalcemia Metabolic acidosis Hyperphosphatemia Reduced absorption through intestinal tract caused by decreased 1,25-(OH)2 D3, inrestinal injury led by toxins, and calcium consumption through combining with phosphate to form calcium phosphate.
Hematologic disorders Anemia decreased EPO production suppression of red cell production by uremic toxins decreased life-span of red blood cell iron deficiency Coagulopothy---bleeding disorder platelet function is impaired, although platelet production is normal.
Hypertension Increased blood volume led by water and sodium retention Decreased levels of renal vasodilator prostaglandins Increased activity of renin-angiotensin system
Treatment Medical management Dialysis and transplantation hemodialysis peritoneal dialysis transplantation Dietary management protein restriction adequate calorie intake (carbohydrate and fat) potassium, sodium and fluid restriction