Management of patients with renal disorders Primary glomerular disease Renal failure

Pathophysiology Primary glomerular disease: Inflammation of glomerular capillaries Antigen-antibody complexes—Deposition of these complexes in glomerular capillaries (IgG)—inducing inflammatory response Major indicators of Glomerular Injury—proteinuria, hematuria, decreased GFR, hypertension, edema, decreased excretion of Na Acute Nephritic Syndrome: clinical manifestations of glomerular inflammation Glomerulonephritis: inflammation of glomerular capillaries that occurs in acute or chronic form

Health assessment clinical manifestations Main manifestations of AGI: Hematuria, edema, azotemia, proteinuria, Hematuria could be microscopic or macroscopic Cola-colored urine because of RBCs Edema & hypertension Proteinuria due to increased permeability of glomerular membrane; with pitting edema Headache, malaise, flank pain In elderly, circulatory overload, with dyspnea, pulmonary edema

AGI Clinical manifestations In acute nephritic syndrome: the kidneys become large & edematous, congested Elevated serum IgA As urine out put decreases, BUN and creatinine in the blood increases Kidney biopsy may be needed If improvement: amount of urine increases; urinary protein diminish Some may develop uremia and require dialysis for survival

Complications Hypertensive encephalopathy: emergency management of hypertension Glomerulonephritis, without treatment, progresses to ESRD: S & S—hematuria, proteinuria Heart failure & pulmonary edema

Nursing management Treat symptoms, preserve kidney function & treat complications:  Antibiotic, Penicillin; if the cause is infection  Corticosteriods; managing HTN; controlling proteinuria  protein restriction, when renal insufficiency and increased BUN  Na restriction, when HTN, edema & HF  Liberal intake of CHOs, to provide energy & reduce catabolism of protein; Intake and output, daily weight,  Fluid based on I & O  Patient education

Chronic glomerulonephritis Secondary to repeated acute nephritic syndrome & other health conditions; hyperlipidemia Kidneys are reduced to one-fifth of normal size—fibrous tissues; cortex shrinks to 1-2 mm in thickness Glomeruli become scarred; renal artery branches are thickened The result is sever glomeruli damage– ESRD May discovered accidentally, when HTN, elevated BUN & Creatinine are detected May report general symptoms: weight loss, increasing irritability, increased need to urinate at night, headache, digestive disturbances

Chronic glomerulonephritis As progresses, develop signs of chronic renal diseases or renal failure: poorly nourished with yellow-gray pigmentation of the skin Periorbital and peripheral edema Normal blood pressure or severe HTN retinal hemorrhage and exudates Anemia-pale mucous membrane Cardiomegaly, gallop rhythm, distended neck veins peripheral neuropathy & neurosensory changes Development of pericarditis; friction rub, pulsus paradoxus

Assessment / diagnostic findings  Urine, fixed specific gravity 1.010, variable proteinuria, urinary casts  When GFR is below 50ml/min Hyperkalemia, decreased K excretion Metabolic acidosis, because of decreased acid secretion Anemia, decreased production of erythropoiesis Hypoalbuminemia – secondary to protein loss Increased serum phosphorous level Decreased calcium, the Ca binds with phosphorus mental changes; and impaired nerve conduction due to electrolyte imbalances & uremia

Management: symptoms management Reduce hypertension: Na & water restrictions, antihypertensives; monitor Wt. daily, diuretics, Protein of high biologic value—dairy products, eggs, meat to promote good nutritional status Adequate calories—spare protein for tissue growth Manage UTI Initiation of dialysis may be required; in the early period of the disease process. Nursing management Monitor fluid & electrolytes imbalances Report system changes reduce anxiety; Emotional support

Nephrotic syndrome A type of renal failure-increased glomerular permeability; is manifested by Massive proteinuria; Hypoalbuminemia; Diffuse edema Hyperlipidemia, increased serum cholesterol & LDL  Caused by intrinsic renal disease or systemic diseases that cause glomerular damage  Major manifestations  Edema, pitting in dependent areas (periorbital), ascites  Irritability, headache,-- malaise

Nephrotic syndrome management Treat underlying disease; slowing progression to CKD Typical treatment include: Diuretics for edema ACE inhibitors to reduce proteinuria Lipid lowering agents Nursing management: Instruct to follow medications & dietary regimen Aware about and communicate health changes

Renal Failure Acute Renal Failure A rapid loss of renal functions related to kidney damage A life-threatening metabolic complications can occur— metabolic acidosis, fluid & electrolyte imbalances Accepted criterion for ARF: 50% or greater increase in serum creatinine; The normal is less than 1 mg/dL Increased BUN Changes in urine volume may occurs Oliguria, less than 500 ml/day Anuria, less than 50 ml/day Non-oliguria, greater than 800 ml/day

ACUTE RENAL FAILURE There is a specific underlying problem Some of these factors—reduce blood flow to the kidney Hypovolemia; hypotension; reduced cardiac output Obstruction by tumor, blood clot, or renal stone Bilateral obstruction of renal arteries or veins Should be treated before permanent damage occur

Categories of ARF Pre renal ARF; is the result of impaired blood flow, causing hypoperfusion and decreasing GFR Intra renal ARF: is the result of actual parenchymal damage to glomeruli or tubules—abnormal reabsorption & decreased urine flow; leading to acute tubular necrosis; intra-tubular obstruction Post renal ARF: obstruction distal to the kidney: pressure rises in the kidney, decreased GFR Read chart 44-4, P

Phases of ARF  The initiation period: begins with insult and ends when oliguria develops  The oliguria period: increase serum concentrations of substances that kidneys excretes Uremic symptoms appear and life-threatening condition, hyperkalemia, develops Some patients have decreased renal function but excrete 2L/day, non-oliguria renal failure; Occurs after exposure to nephrrotoxic agents, burn, trumatic injury

Phases of ARF  The diuresis period: gradual increase in urine—glomerular filtration starts to recover renal function may still abnormal; because uremic symptoms present—thus, needs expert attention Observe for dehydration  The recovery period: Signals improvement of kidney function; may need 3-12 months; lab values return to normal Leave 1-3% reduction in the GFR—not clinically significant

Assessment Appears critically ill & lethargic; dry skin; dehydration CNS symptoms: drowsiness, headache, seizures Urine output: scant to normal; hematuria may be present Low specific gravity indicating inability to concentrate, a sign of tubular damage; an early sign Pre renal azotemia—decreased urinary Na to less than 20 mEq/L; Intra renal azotemia—urinary Na more the 40 mEq/L Increased BUN and creatinine Hyperkalemia with oliguria or anuria; metabolic acidosis, can not excrete acid metabolites phosphate high and calcium low—decreased absorption from GIT; Anemia; CT, MRI or ultrasonography

Prevention of ARF Careful history to identify exposure to nephrotoxic agents, medications: Blood tests for BUN & creatinine, 24 hours after initiation of nephrotoxic medications and 2 times a week Adequate hydration for those at risk for dehydration Prevent & treat shock promptly For critically ill patients; monitor CVP, arterial pressure, urine output Treat hypotension promptly Prevent & treat infections READ CHART 44-5, P 1322

Management principles  Treat the underlying cause: pre renal azotemia by optimizing renal perfusion, post renal failure with removing obstruction, intra renal azotemia with supportive therapy; with Removal of causative agents, Aggressive management of pre and post-renal failure Avoidance of associated risk factors Prompt treatment of shock and infection