lecture kidney pathophysiology презентация

functions: - Participate in maintaining consistency and osmolarity of the extracellular fluid concentrations of various electrolytes in it (Na \ K +, Ca +P, etc.); - Excrete metabolic products and many exogenous compounds; - Regulate systemic arterial pressure; - regulate the acid-base status, maintaining the consistency buffer bases plasma and H +; - Secrete erythropoietin, which stimulates erythropoiesis; - Form the active form of vitamin D3.

Urine formation Glomerular Filtration. Tubular Reabsorption Tubular Secretion.

Glomerular Filtration. As blood flows through the glomeruli, much of its fluid, containing useful chemicals and dissolved waste materials, soaks out of the blood through the membranes (by osmosis and diffusion) where it is filtered and then flows into the Bowman's capsule. This process is called glomerular filtration. The glomerular filtrate consists of water, excess salts (primarily Na+ and K+), glucose, and a waste product of the body called urea. The total rate of glomerular filtration (glomerular filtration rate or GFR) is normally about 125 ml per minute.

Glomerular Filtration. The glomerulesfiltation  can be decreased or increased. filtration decrease: 1.Hydrostatic pressure decrease in glomerules capillaries: in general decreasing  of arterial pressure decrease,  aorta and kidneys arteries organic defeats , kidneys arteries thrombosis or embolism. 2. Plasma oncotic pressure increase – protein blood substitutes transfusion in large volumes . 3. Intrakidney pressure increase –  canalicules or urinary tract block with stones. 4.  Glomerulus filter disorder – quantity functioning glomerulus decrease

Glomerular Filtration. The increase in the volume of glomerular filtrate. Causes. - Improving the efficiency of the filtration pressure by increasing the tone of the smooth muscle cell efferent arterioles (under the influence of catecholamines, Pg, angiotensin, ADH) or decreased tone smooth muscle cell bringing arteriol (exposed to kinins, Pg, and others.), Plasma oncotic pressure decrease (liver failure , starvation, prolonged proteinuria). - Increase filtration barrier permeability (due to the disintegration of the basement membrane) under the influence of biologically active substances - mediators of inflammation or allergy (histamine, kinins, hydrolytic enzymes).

Tubular Reabsorption Is the movement of substances out of the renal tubules back into the blood capillaries located around the tubules. Substances reabsorbed are water, glucose and other nutrients, sodium (Na+) and other ions. Disorder of the tubular function is called as tubular  insufficiency. It can be hereditary or acquired..

Tubular Secretion. Nephron tubule cells have the added capacity to extract materials from blood of the peritubular capillaries and secrete them directly into urine. These substances are secreted through either an active transport mechanism or as a result of diffusion across the membrane. Substances secreted are hydrogen ions (H+), ammonia (NH3), and certain drugs. Kidney tubule secretion plays a crucial role in maintaining the body's acid-base balance.

Changes in the composition of urine. Proteinuria. Normally, the penetration of plasma proteins into glomerular filtrate inhibit glomerular filter . In a healthy human plasma in the glomeruli of filtered 0.5 g of protein per day (mainly albumin). A large part of incoming protein in the glomerular filtrate is reabsorbed in the proximal tubules by means of pinocytosis. The total amount of protein released from the daily urine, normally about 50 mg. Urinary excretion of more than 50 mg of protein per day called proteinuria. On the mechanism of development distinguish glomerular and tubular proteinuria.

Glomerular proteinuria is associated with increased permeability of the glomerular filter, tubular - in violation of the protein reabsorption in the proximal tubule epithelium due to lack of function or reduce the outflow of lymph from the kidney tissue.

Hematuria (red blood cell) - a pathological phenomenon, characterized by an excess (higher than normal) urinary excretion of red blood cells. Mechanism hematuria in various diseases of the kidneys and urinary tract are not the same. 1. Renal hematuria due to: a decrease in the negative charge of red blood cells of peripheral blood, damage (fragmentation) of red blood cells in patients with renal and generalized mikroapgiopatii, increased vascular permeability of glomerular capillaries and peritubular capillaries, reducing the electric charge of the basement membrane of glomerular capillaries, in hemorrhagic vasculitis, thrombocytopenia, hemophilia, overdose of anticoagulants reason hematuria- decrease clotting activity. 2. When urolithiasis occurrence of hematuria associated with damage to the mucosa of the ureter or bladder concrement. 3. In patients with tuberculosis, kidney tumors and bladder hematuria is caused by the destruction of tissues and damaged blood vessels in it. 4. urological pathology cause of hematuria can be venous hypertension.

Diseases of the kidneys are divided into 2 major groups according to the predominant involve­ment of morphologic components: Diseases of the kidneys are divided into 2 major groups according to the predominant involve­ment of morphologic components: Glomerular diseases. 2. Tubulointerstitial diseases. Glomerular diseases encompass a large and clinically significant group of renal diseases. Glomerular diseases are divided into 2 groups: I. Primary glomerulonephritis in which the glomeruli are the predominant site of involvement(Glomerulonephritis). II. Secondaryglomerular diseases include certain systemic and hereditary diseases which secondarily affect the glomeruli.

ACUTE NEPHRITIC SYNDROME. The nephritic syndrome is the result of disturbance of glomerular structure that involves reactive cellular proliferation. This causes reduced glomerular blood flow (leading to reduced urine output- oliguria), leakage of red cells from damaged glomeruli (haematuria), and consequent retention of waste products (uraemia). The low renal blood flow activates the renin- angiotensin system, with fluid retention and mild hypertension. Small amounts of proteins are also lost in the urine, but this is usually trivial. The haematuria is not gross and is usually manifest as a smoky brown discoloration of urine.

NEPHROTIC SYNDROME Nephrotic syndrome is a group of diseases having different pathogenesis and characterized by clinical findings of massive proteinuria (>3.5 g/day) and lipiduria, hypoalbuminemia (<3 g/dL), generalized edema, and hyperlipidemia. The nephrotic syndrome is caused by disorders that increase the permeability of the glomerular capillary membrane, causing massive loss of protein in the urine.

Odema results from salt and water retention and a loss of serum albumin below that needed to maintain the osmotic pressure of the vascular compartment. The sodium and water retention appears to be caused by several factors, including a compensatory increase in aldosterone, stimulation of the sympathetic nervous system, and a reduction in secretion of natriuretic factors. As a resultloss immunoglobulin’s and complements components in the urine, persons with nephritic syndrome are predisposed to infections.

The hyperlipidemia is characterized by elevated levels of triglycerides and low-density lipoproteins (LDL). These abnormalities are increased synthesis of lipoproteins in the liver secondary to a compensatory increase in albumin production. Because of the elevated LDL levels, persons with nephrotic syndrome are at increased risk for development of atherosclerosis.

Hypercoaguability. At nephrotic syndrome may develop thrombosis as a result of various factors. These include: increased urinary loss of antithrombin III, hyperfibrinogenaemia due to increased synthesis in the liver, decreased fibrinolysis, increased platelet aggregation. Thrombotic complications include deep vein thrombosis and pulmonary emboli.

tubulointerstitial pathology. Damage to tubulointerstitial tissues results in alterations in reabsorption and secretion of important constituents leading to excretion of large volumes of dilute urine., Tubulointerstitial diseases can be categorised according to initiating etiology into 4 groups: Vascular causes: Long-standing primary or essential hypertension produces characteristic changes in renal arteries and arterioles referred to as nephrosclerosis Infectious causes: A good example of chronic renal infection causing CRF is pyelonephritis. Toxic causes: Some toxic substances induce slow tubular injury. The most common example is intake of high doses of analgesics such as phenacetin, aspirin and acetaminophen (chronic analgesic nephritis). Obstructive causes: Chronic obstruction in the urinary tract leads to progressive damage to the nephron due to fluid back-pressure. The examples of this type of chronic injury are stones, tumours, strictures.

ACUTE RENAL FAILURE Acute renal failure represents a rapid decline in renal function sufficient to increase blood levels of nitrogenous wastes and impair fluid and electrolyte balance. The most common indicator of acute renal failure is azotemia, an accumulation of nitrogenous wastes (urea nitrogen, uric acid, and creatinine) in the blood. In acute renal failure the glomerular filtration rate (GFR) is decreased. As a result, excretion of nitrogenous wastes is reduced and fluid and electrolyte balance cannot be maintained

The causes of acute renal failure Prerenal failure, the most common form of acute renal failure, is characterized by a decrease in renal blood flow. It is reversible if the cause of the decreased renal blood flow can be identified and corrected before kidney damage occurs. Causes of prerenal failure include depletion of vascular volume (hemorrhage), impaired perfusion caused by heart failure and cardiogenic shock, and decreased vascular filling because of increased vascular capacity (e.g., anaphylaxis or sepsis). Postrenal failure results from obstruction of urine outflow from the kidneys. The obstruction can occur in the ureter (i.e., calculi and strictures), bladder (i.e., tumors or neurogenic bladder), or urethra (i.e., prostatic hypertrophy). Intrarenal renal failure results from conditions that cause damage to structures within the kidney—glomerular, tubular, or interstitial. Injury to the tubules is most common and often is ischemic or toxic in origin. The major causes of intrarenal failure are ischemia associated with prerenal failure, toxic insult to the tubular structures of the nephron, and intratubular obstruction. Acute glomerulonephritis and acute pyelonephritis also are intrarenal causes of acute renal failure.

3 stages Oliguric stage: is characterized by urinary output of less than 400 ml per day, causing sudden retention of endogenous metabolites such as urea, potassium, sulfate, and creatinine that normally are excreted by the kidneys. Fluid retention gives rise to edema, water intoxication, and pulmonary congestion. If the period of oliguria is prolonged, hypertension frequently develops and with it manifestation of uremia. When untreated, the neurologic manifestations of uremia progress from neuromuscular irritability to somnolence, coma, and death ii) Diuretic stage: the period during which repair of renal tissue takes place. Its usually a gradual increase in urine output and a fall in serum creatinine, indicating that the nephrons have recovered. Diuresis often occurs before renal function has fully returned to normal. BUN and serum creatinine, potassium, and phosphate levels may remain elevated or continue to rise. In some cases, the diuresis may result from impaired nephron function and may cause excessive loss of water and electrolytes. iii) stage of recovery: Full recovery with healing of tubu­lar epithelial cells occurs in about half the cases. The process of healing may take up to one year with restoration of normal tubular function.

Chronic renal failure is a syndrome characterised by progressive and irreversible deterioration of renal function due to slow destruction of renal parenchyma, eventually terminating in death when sufficient number of nephrons have been damaged. Chronic renal failure can result from a number of conditions that cause loss of nephrons, including diabetes, hypertension, glomerulonephritis.T he symptoms of renal failure occur gradually and do not become evident until the disease is far advanced. Chronic renal failure results in progressive deterioration of glomerular filtration, tubular reabsorptive capacity, and endocrine functions of the kidneys.

1.Decreased renal reserve. At this stage, damage to renal parenchyma is marginal and the kidneys remain functional. The GFR (glomerular filtration rate) is about 50% of normal, BUN (blood urea nitrogen) and creatinine values are normal and the patients are usually asymptomatic except at times of stress. 1.Decreased renal reserve. At this stage, damage to renal parenchyma is marginal and the kidneys remain functional. The GFR (glomerular filtration rate) is about 50% of normal, BUN (blood urea nitrogen) and creatinine values are normal and the patients are usually asymptomatic except at times of stress. 2. Renal insufficiency. At this stage, about 75% of functional renal parenchyma has been destroyed. The GFR is about 25% of normal accompanied by elevation in BUN and serum creatinine. As nephrons are destroyed, the remaining nephrons compensate for those that are lost by filtering more solute particles from the blood. Because the solute particles are osmotically active, they cause additional water to be lost in the urine. One of the earliest symptoms of renal insufficiency is isosthenuria with urine that is almost isotonic with plasma. Renal failure. At this stage, about 90% of functional renal tissue has been destroyed. The GFR is about 10% of normal. Tubular cells are essentially nonfunctional. As a result, the regulation of sodium and water is lost resulting in oedema, metabolic acidosis, hypocalcaemia, and signs and symptoms of uraemia. 4. End-stage kidney. The GFR at this stage is less than 5% of normal. Uremia, which means “urine in the blood,” is the term used to describe the clinical manifestations of ESRD. Uremia differs from azotemia, which merely indicates the accumulation of nitrogenous wastes in the blood and can occur without symptoms.