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(oliguria and uraemia and accumulation of nitrogenous wastes in the body). As a result there can be leakage of blood cells, protein and other needed substances from damaged glomerulus. Acute nephritis usually has a good prognosis but a few patients progress to chronic...

(oliguria and uraemia and accumulation of nitrogenous wastes in the body). As a result there can be leakage of blood cells, protein and other needed substances from damaged glomerulus. Acute nephritis usually has a good prognosis but a few patients progress to chronic nephritis. Usually chronic nephritis is asymptomatic. But as the disease progresses, the patient can die from hypertension and renal failure. DISEASES AFFECTING THE KIDNEYS AND URETERS ACUTE GLOMERULONEPHRITIS DEF 1- Acute glomerulonephritis is the inflammation of the glomeruli of the kidneys. (the capillaries that filter substances from the plasma). DEF 2-Inflammation of the glomeruli capillaries. AETIOLOGY Group A beta-hemolytic Streptococcal infections of the throat may precede the onset of glomerulonephritis by 2 to 3 weeks /the disease occurs 2-3 weeks after a streptococcal infection of the throat. Sometimes it is called acute post streptococcal glomerulonephritis. It may also occur after any skin infection such as impetigo (a contagious skin disorder caused by streptococci or staphylococci or a combination of organisms and is marked by vesicles or bullae that becomes pustular, rupture and form yellow crusts). 32  Bacterial Endocarditis Acute viral infections (upper respiratory tract infections such as mumps, varicella zoster virus, Epstein-Barr virus) Hepatitis B Human immunodeficiency virus [HIV] infection Schistosomiasis also called Bilharzia Leishmaniasis- Immunologic abnormalities Free radicals-radicals that carry an unpaired electron, such radicals are extremily reactive Vascular disorders In some patients, antigens outside the body (eg, medications, foreign serum,toxins) initiate the process, resulting in antigen–antibody complexes being deposited in the glomeruli.In some patients the kidney itself will serve as the inciting antigen. PATHOPHYSIOLOGY Acute glomerulonephritis is often initiated by activation of the client’s immunologic response mechanisms. The antigen that activates the immune response may be Endogenous or Exogenous Endogenous antigen may already be present in the glomerulus or other tissues such as the 33 nasopharynx, blood vessels or joints. Exogenous antigens are usually derived from infections-viruses, bacteria, fungi and parasites. The formation of antibodies in response to antigen stimulation results in several events that leads to injury. When an antigen usually Group A-beta haemolytic streptococcus is found in the body, the immune system produces an antibody against the antigen. Consequently there is the deposition of antigen-antiboby complex ( in the glomerulus. The results is increased production of epithelial cells lining the glomerulus (cellular proliferation).Leukocytes or white blood cells, then infiltrate the glomerulus resulting in thickening of the glomerular filtration membrane.Scarring and loss of GFM occurs and this gives rise to Decreased glomerular filtration rate( less than 125-200ml/minute).  Antigen (Group A beta hemolytic streptococci)  Antigen – antibody products (IgG- anti-IgG immune complexes)  Deposits of antigen - antibody complex in the glomerulus  Increased products of epithelial cells lining the glomerulus (cellular proliferation)  Leukocytes proliferation and infiltration of glomerulus  Thickening of glomerular membrane  Scarring and loss of glomerular filtration membrane  Decreased glomerular filtration rate (GFR) 34  CLINICAL MANIFESTATIONS - The primary presenting feature of acute glomerulonephritis is hematuria (blood in the urine), the earliest sign and is almost universal, which may be microscopic (identifiable through microscopic examination) or macroscopic or gross (visible to the eye). The urine may appear cola-colored because of RBCs and protein plugs or casts. (RBC casts indicate glomerular injury.) - Proteinuria (primarily albumin), this is present, due to the increased permeability of the glomerular membrane./Foamy urine appearance - BUN and serum creatinine levels may rise as urine output drops. The patient may be anemic. -Generalized oedema especially around the eyes, feet or ankles -Reduced urine volume or oliguria -Hypertension is noted in 75% of cases -Azotemia -Protein Plug/casts in urine Headaches 35  Malaise Flank pain Elderly patients may experience circulatory overload with dyspnea, engorged neck veins, cardiomegaly pulmonary edema. DIAGNOSTIC MEASURES History, signs and symptoms Serum IgA may be elevated in some patients Kidney biopsy Urinalysis Urine culture Blood Urea Nitrogen > Erythrocyte Sedimentation Rate MEDICAL MANAGEMENT 36  The medical management depends on the cause of acute glomerulonephritis Residual Streptococci infections e.g penicillin is the agent of choice but other broad spectrum antibiotics may be prescribed Corticosteroids and immune-suppressants to control inflammation may be prescribed for patients with rapidly progressive acute glomerulonephritis (prednisolone) Loop diuretics and antihypertensive agents may be prescribed to control severe hypertension. e.g. Lasix Dialysis may be indicated in acute glomerulonephritis if azotemia and or uremic symptoms are present. NURSING MANAGEMENT For clients with oliguria fluid intake is restricted and diet modifications may be necessary. The usual fluid allowance is that equal to the urinary output plus 500 to 600ml to account for insensible losses (fluid loss through the respiratory and GI tracts) In clients with oliguria, there is usually urinary retention of sodium and potassium and elevation of blood Urea Nitrogen(BUN) level. Potassium and protein intake must be restricted to prevent hyperkaliemia and additional uraemic manifestations of the elevated BUN. A low-sodium diet may be needed to control hypertension and oedema. Monitor fluid intake and output Monitor weight and blood pressure regularly 37  Restrict sodium and protein intake Ensure adequate carbohydrate intake to provide energy and prevent breakdown of protein Teach client the signs of infection and the need to seek early treatment Educate on early signs of complications such as headaches, unexplained weight gain and the need to report. COMPLICATIONS Hypertensive encephalopathy Heart failure Pulmonary oedema End stage renal failure with uraemia CHRONIC GLOMERULONEPHRITIS DEF- Chronic glomerulonephritis is a slow progressive inflammation of the glomeruli causing irreversible damage to the nephrons. DEF 2-Refers to renal deterioration or renal failure that develops over a period of years (20-30yrs) or even longer. AETIOLOGY 38  In most cases the exact onset of the disease is rarely identified because the kidneys are atrophied and tissue may not be available for biopsy or diagnosis. There may be no history of renal disease before the diagnosis. Although the exact pathogenesis is not known, the changes in the renal parenchyma may result from the following; May be due to repeated episodes of acute glomerulonephritis. Hypertensive nephrosclerosis /the effect of hypertension-hypertension with sclerosis of renal arterioles may be present. Hyperlipidemia or hypercholesterolaemia Tubule interstitial injury (chronic) The renal manifestation of systemic diseases such as Systemic Lupus Erythematosis,Goodpastures syndrome. Diabetic glomerulosclerosis Amyloidosis Glomerular injury results in proteinuria because of increased permeability of the glomerular basement membrane. PATHOPHYSIOLOGY Chronic inflammation leads to increasing bands of scar tissues that replaces the normal nephrons. 39  scar tissue distort the remaining cortex, making the surface ofthe kidney rough and irregular. Kidneys are reduced as little as 1/5 of their normal size consisting largely of fibrous tissue The cortex shrinks to a layer 1 to 2 mm thick or less Glomerular filtration rate progressively reduces as numerous glomeruli and their tubules become scared and branches of the renal artery become thickened causing severe glomerular damage. CLINICAL MANIFESTATION Mild proteinuria, hematuria, hypertension and occasional oedema are the only manifestations. Because bleeding can occur anywhere along the urinary tract, the characteristics of haematuria from red blood cells escaping through the glomerular membrane include smoky brown- tinged urine,red blood cell casts and an accompanying proteinuria., protein exceeding 3-5g/day with albumin as the major protein. Patients may not show any s/s until Blood Pressure, BUN and creatinine get elevated The diagnosis may be suggested during a routine eye examination when vascular changes or retinal hemorrhages are found. During routine eye exams with vascular damage/ bleeding may be identified 40  The first indication of the disease may be a sudden severe nose bleed, a stroke or a seizure may be the first sign Many patients report that their feet are slightly swollen at night - Pedal edema especially at night As the disease progresses signs and symptoms of renal insufficiency and chronic renal failure may develop; The patient appears poorly nourished /signs of malnutrition Periorbital and Peripheral oedema may develop Blood Pressure may be normal or severely elevated Mucous membranes are pale because of anaemia Cardiomegaly, distended neck veins and other signs of heart failure may be present. Crackles can be heard in the lungs Nocturia Confusion DIAGNOSTIC MEASURES 41  Urinalysis  Specific gravity of urine 1.010-This is fixed  Proteinuria-may be variable  Urinary cast- protein plugs secreted by damaged kidney tubules  Decreased GFR below 50ml/min (Normal-125-200ml/min) Hyperkalaemia - decreased excretion of potassium Metabolic acidosis from decreased acid excretion by kidney Anaemia due to decreased erythropoiesis for production of RBCs Hypoalbuminemia due to protein loss Increased serum phosphorus due to decreased renal excretion of phosphorus Decreased serum calcium level – calcium binds to phosphorus to compensate for elevated serum phosphorus levels Chest X-rays show cardiac enlargement ECG – left ventricular hypertrophy or normal CT scans and MRI show decreased renal cortex MEDICAL MANAGEMENT Management for patients with chronic glomerulonephritis is largely symptomatic. 42   If the patient has hypertension, the blood pressure is reduced with sodium and water restriction, antihypertensive agents, or both.  Weight is monitored daily, and diuretic medications are prescribed to treat fluid overload.  Proteins of high biologic value such as dairy products, eggs, meats are provided to promote good nutritional status.  Adequate calories are also important to spare protein for tissue growth and repair.  Urinary Tract Infections must be treated promptly to prevent further renal damage  Antibiotics to treat urinary tract infections  Antihypertensive  Diuretics  Dialysis NURSING INTERVENTION Serve protein of high biologic value (dairy products, eggs) and aadequate calories Monitor fluid intake and output-clients pattern of voiding is noted –changes in colour, odor or clarity of the urine. Assess for changes in behavior as uraemia can cause behavior change The nurse assesses client’s ability to pursue activities such as reading, job related functions or other processes requiring mental concentration (changes in memory or the ability to 43  concentrate occur with accumulation of waste products that accompanies renal failure. Assess for altered fluid and electrolyte balance Assess for signs of Renal Failure e.g. nausea, vomiting, decreased urine output Give emotional support to client and family Consistent follow up by clients to control hypertension is of necessity. Client should avoid nephrotoxic agents The nurse inspects the clients skin for a yellowish colour,ecchymoses,and rashes or eruptions.The skin is examined for texture and the nurse notes areas of dryness and breaks that might have resulted from scatching. The nurse inspects the neck veins to identify venous engorgement and also checks for pedal oedema. The nurse notes whether client has slurred speech,ataxia or tremors. COMPLICATIONS Acute kidney failure Chronic Kidney Disease Hypertension Nephrotic syndrome 44