By Linda Self

      Regulation of water excretion Regulation of electrolyte function Regulation of acid-base balance—retain HCO3- and excrete acid in urine Regulation of blood pressure--RAAS Regulation of RBCs Vitamin D synthesis

  Secretion of prostaglandin E and prostacyclin which cause vasodilation, important in maintaining renal blood flow Excretion of waste products-body’s main excretory organ. Urea, creatinine, phosphates, uric acid and sulfates. Drug metabolites.

Stimuli for Renin Excretion Angiotensinogen in liver Renin release Angiotensin I Converting enzyme in lungs Angiotensin II Renal autoregulation Increased BP, increased circulating volume

      Renin—raises BP Bradykinins—increase blood flow and vascular permeability Erythropoietin ADH Aldosterone—promotes sodium reabsorption and potassium excretion Natriuretic hormones—released from the cardiac atria and brain.

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Hypertension Diabetes mellitus Immobilization Parkinson’s disease SLE Gout Sickle cell anemia, multiple myeloma BPH Pregnancy SCI

      GFR decreases following 40 years with a yearly decline of about 1 mL/min Renal reserve declines Multiple medications can result in toxic metabolites Diminished osmotic stimulation of thirst Incomplete emptying of bladder Urinary incontinence

      Sp. Gravity—1.005-1.020

Microscopic examination for protein, RBCs, ketones, glycosuria, presence of bacteria, general appearance and odor Leukocyte esterase—enzyme found in WBCs Nitrites –bacteria convert nitrates to nitrites Osmolality—accurate measurement of the kidney’s ability to concentrate urine. Normal range is 500-1200 mOsm/kg. Culture important in ‘Id’ing pathogen

   Albuminuria—albumin in urine not measurable by dipstick Normal values in freshly voided sample should range between 2.0-20 for men and 2.8-28 for women. Higher levels indicate microalbuminuria.

Can also be determined by 24h specimen

    Urine osmolality—indication of concentrating ability, changes seen early in disease processes Creatinine clearance—tests clearance of creatinine in one min. Reflects GFR.

Serum creatinine—measures effectiveness of renal function. 0.6 to 1.2 mg/dL Urea nitrogen—also indicator of renal function. 7-18 mg/dL. Measures renal excretion of urea nitirogen, a byproduct of protein metabolism. Is not always elevated with kidney disease. Not best indicator of renal function.

  Liver must function properly to produce urea nitrogen. BUN levels indicate the extent of renal clearance of this nitrogenous waste product.

May see elevation of BUN with bleeding into tissues or from rapid cell destruction from infection/steroids

   Ratio of BUN to creatinine distinguishes between renal and non-renal factors causing elevations Dehydration can affect the BUN When blood volume is down, or BP is low, BUN level rises more rapidly than creatinine level.

   Volume of fluid filtered from renal glomerular capillaries into Bowman’s capsule per unit of time Generally expressed in ml/minute Normal GFR generally is 125mL/minute

    Cockcraft-Gault formula Modification of Diet in Renal Disease Study Group formula (MDRD) Schwartz formula Starling equation

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No common pathologic condition, other than renal disease, increases the serum creatinine level

Serum creatinine does not increase until at least 50% of renal function is lost

   Is a calculated measure of glomerular filtration rate. Is best indicator of overall kidney function.

Based on 24 hour urine collection Midway will obtain serum creatinine. Serum creatinine levels vary with age, gender and body muscle mass  Calculate: (Volume of urine X urine creatinine) Divided by serume creatinine

       KUB Ultrasonography CT MRI Nuclear scans IV urography—IVP. NPO before. Bowel prep. Nephrotoxic agent. Metformin.

VCUG

    Cystoscopy Ureteral brush biopsy Kidney biopsy Urodynamic tests—cystometrogram. Measures detrusor muscle function.

     Antigen-antibody complexes form in blood and become trapped in glomerular capillaries Induce an inflammatory response Manifested by proteinuria, hematuria, decreased GFR and alteration in excretion of sodium Acute and chronic glomerulonephritis Nephrotic syndrome

Antigen (group A strep) Antigen-antibody product Deposition of antigen-antibody complex in glomerulus Increased production of epithelial cells lining the glomerulus Leukocyte infultration of the glomerulus Thickening of the glomerular filtration membrane Scarring and loss of glomerular filtration membrane Decreased GFR

 Staph, klebsiella, CMV, mono, hep B, mycoplasma, group A beta-hemolytic strep

        Hematuria Edema Azotemia-accumulation of nitrogenous wastes Urine appearance may be cola colored Hypertension Hypoalbuminemia Hyperlipidemia Rising BUN and creatinine

   Hypertensive encephalopathy Heart failure Rapid decline in renal function can occur to ESRD

         Treat s/s such as elevated BP Check GFR by 24h urine for creatinine clearance ANA Treat streptococcal infection with antibiotics, preferably PCN Corticosteroids Immunosuppressants Limit dietary protein, increase CHO Restrict sodium May progress to chronic glomerulonephritis, will treat as in CKD

      Is not a specific glomerular disease Is a syndrome with a cluster of findings that include: Marked increase in protein in urine (especially albumin) Hypoalbuminemia Edema High serum cholesterol and LDL

      A condition of increased glomerular permeability Results in massive protein loss Often linked genetically or r/t immune/inflammatory process Caused by chronic glomerulonephritis, diabetes mellitus with glomerulosclerosis, amyloidosis, lupus, multiple myeloma and renal vein thrombosis Major manifestation is edema Hallmark is albuminuria exceeding 3.5g/day

Damaged glomerular cap. membrane Loss of plasma protein (albumin) Stimulates synthesis of lipoproteins hyperlipidemia

Damaged glomerular capillary membrane Loss of plasma proteins hypoalbuminemia Decreased oncotic pressure Generalized edema>RAAS>sodium retention>>>>edema

       Massive proteinuria Hypoalbuminemia Edema Lipiduria Hyperlipidemia Increased coagulation Renal insufficiency

       Renal biopsy to determine specific cause Steroids Immunosuppressive agents ACEIs can decrease proteinuria Cholesterol lowering agents Heparin to reduce coagulability Limit sodium intake

   Reversible clinical syndrome whereby there is sudden and pronounced loss of kidney function Occurs over hours to days Results in kidneys failure to excrete nitrogenous wastes

Intrarenal actual parenchymal damage  Prolonged renal ischemia from myoglobinuria (rhabdo, trauma, burns), hemoglobinuria (transfusion reaction, hemolytic anemia)  Nephrotoxic agents like aminoglycosides, radiopaque contrast, heavy metals, solvents, NSAIDs, ACEIs, acute glomerulonephritis

Prerenal 60-70% of cases  Volume depletion as seen in hemorrhage, renal losses from diuretics, GI losses from vomiting, diarrhea   Impaired cardiac output 2ndary to MI, heart failure, dysrhythmias, cardiogenic shock Vasodilation from sepsis, anaphylaxis, antihypertensive meds

Postrenal

Urinary tract obstruction by calculi, tumors, BPH, blood clots

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Initiation occurs with the insult Oliguria with urinary output less than 400ml/24h . rising potassium, BUN, Cr. Not responsive to fluid challenges.

Diuresis period— gradual increase in urinary output. Beginning recovery. Renal function gradually improves Recovery—may take 3-12 months. May have permanent reduction in functioning of 1%-3%.

  Prerenal-hypotension, tachycardia, decreased CO, decreased urinary output, lethargy intrarenal and postrenal—oliguria or anuria, hypertension, tachycardia, SOB, orthopnea, n/v, generalized edema and weight gain, lethargy, confusion

 Nonoliguric form also exists. Phases are similar.

       Elevated BUN and creatinine Sodium retention but may be deceptive due to water retention Potassium increased Phosphorus increased Calcium decreased H&H decreased Sp. Gravity decreased and fixed

 Objectives : Restore normal chemical balance and prevent complications until restoration of renal function  Identify and treat underlying cause  Maintain fluid balance—wts, serial CVP readings, BP, strict I&O   May give Mannitol, Lasix or Edecrin May need temporary dialysis

  If prerenal, fluid challenges and diuretics to enhance renal blood flow Oliguric renal failure, low dose dopamine. Calcium channel blockers may be used to prevent influx of calcium into kidney cells, maintains cell integrity and increase GFR

      Hyperkalemia—closely monitor electrolytes Kayexalate/Sorbitol—may need Flexiseal IV dextrose, insulin and calcium may help shift K+ Cautious administration of any medication that can be nephrotoxic Monitor ABGs and acid-base balance Monitor phosphate levels

    Azotemia and uremia are directly related to the rate of protein breakdown Dietary proteins are individualized to each patient. Is a catabolic state and if insufficient intake, patient may lose up to 0.5-1 pounds daily. Encourage high CHO. Protein needs for non-dialysis patients need 0.6g/kg of body weight Dialysis patients will need 1-1.5g/kg Fluid restriction=urine volume plus 500ml

      Monitor fluid and electrolyte balance Reduce metabolic demands Promote pulmonary function Prevent infection Provide skin care Provide support

   Progressive, irreversibe deterioration in renal function Causation: #1 diabetes mellitus, hypertension, glomerulonephritis, pyelonephritis, polycystic kidney disease, vascular disorders, others Uremia---collection of nitrogenous wastes normally excreted by the kidneys. S/S include: HA, seizures, coma, dry skin, rapid pulse, elevated BP, scanty urine, labored breathing

      Nephrons hypertrophy and work harder until 70-80% of renal function is lost Nephrons could only compensate by decreasing water reabsorption thus: Hyposthenuria—loss of urine concentrating ability occurs Polyuria—increased urine output Then isosthenuria—fixed osmolality Gradual decline in urinary output

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GFR greater than or equal to 90mL/min/1.73 m2. Kidney damage w/normal or increased GFR GFR = 60-89, mild decrease in GFR GFR = 30-59, moderate decrease in GFR GFR = 15-29. severe decrease in GFR GFR < 15. Kidney failure

      Every body system is affected CV—hypertension (RAAS), heart failure, pulmonary edema, pericarditis, MI Pulm.—crackles, Kussmaul, pleuritic pain Derm—severe pruritus, uremic frost (urea crystals) GI—n/v, anorexia, uremic fetor (ammonia odor to breath), constipation or diarrhea Neurologic—LOC changes, confusion, seizures, agitation, neuropathies, RLS

   Hematologic—anemia, thrombocytopenia Musculoskeletal—muscle cramps, renal osteodystrophy, bone pain, bone fractures Metabolic changes—urea and creatinine, sodium, potassium, acid-base, calcium and phosphorus

      Calcium and phosphorus binders—Calcium carbonate, calcium acetate Antihypertensives Antiseizure—valium or dilantin Erythropoietin Iron supplements Diet—CHO and fat, vitamins, restrict protein

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Uremia 2.

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Persistent hyperkalemia Uncompensated metabolic acidosis 4.

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Fluid volume excess Uremic encephalopathy Remove toxic substances

    Based on principles of diffusion, osmosis and ultrafiltration Diffusion—removal of toxins and wastes. Move from blood to dialysate.

Osmosis—excess water is removed. Goes from area of higher solute concentration (blood) to lower concentration (dialysate) Ultrafiltration—water moves from high pressure area to lower pressure. Applied by negative pressure, more efficient than just by osmosis

          ASHD Disturbances of lipids worsened by dialysis Anemia and fatigue Gastric ulcers Renal osteodystrophy Sleep problems Hypotension Muscle cramps Dysrhythmias Dialysis equilibrium from cerebral fluid shifts

    Caused by rapid decrease in fluid volume and blood urea nitrogen levels during HD Change in urea levels can cause cerebral edema and increased ICP Neurologic complications include: HA, vomiting, restlessness, decreased LOC, seizures, coma or death Can be prevented by starting HD for short periods and low blood flows

   Hemodialysis In ICUs where patient is too unstable to have hemodialysis, can have CRRT Peritoneal dialysis

     More successful if done before dialysis HLA and ABO compatibility Donor kidney placed in iliac fossa Patient must be free from infection Similar care for patient post-op as any surgery

    Post-op—assess for s/s of rejection such as oliguria, edema, fever, increasing blood pressure, weight gain and swelling or tenderness over transplanted area Monitor creatinine level, in those on cyclosporine, may be the only s/s Monitor WBCs Monitor urinary output, may need hemodialysis temporarily (2-3 weeks may initially have ATN)

  Occurs in types 1 and 2 Severity of diabetic renal disease is related to extent, duration and effects of atherosclerosis, htn and neuropathy.

    Microvascular complication of diabetes First manifestation is persistent albuminuria Diabetic patients are always considered to be at risk for renal failure Avoid nephrotoxic agents and dehydration

  Stage 1—at time of diagnosis of diabetes. Kidney size and GFR are increased. Blood sugar control can reverse the changes.

Stage 2, 2-3 years after diagnosis. Basement membrane changes result in loss of filtration surface area and scar formation. These changes are called glomerulosclerosis.

   Stage 3, 7-15 years after diagnosis. Microalbuminuria is present. GRF may be normal or increased.

Stage 4, albuminuria is detectable by dipstick. GRF decreased. BP is increased. Retinopathy is present.

Stage V, GFR decreases at an average rate of 10ml/min./year

  Cystitis Ureterovesical reflux

         If bacteriuria, following should have cultures done: All men All children Patients with diabetics Those with recent instrumentation Those hospitalized or who live in long term care Pregnant women Sexually active Postmenopausal

        Obstruction Stones Diabetes mellitus Gender Age—anticholinergics, neuromuscular conditions, hypoestrogenism Sexual activity Alkalotic urine Vesicoureteral reflux

  Most common organism is E. coli Other causative organisms are: S. saprophyticus,

K. pneumoniae, Proteus and Enterobacter

    Bactrim, Macrodantin, Cipro,Levaquin Fluids, avoid urinary irritants Hygiene Prevention

Acute pyelonephritis

  Will have fever, chills, leukocytosis, bacteriuria and pyuria CVA tenderness   US or CT to r/o any obstruction Urine C&S

      Tx: Hydration Antiemetics Two week course of antibiotics such as Bactrim, Cipro, gentamycin w/or w/o ampicillin, 3 rd generation cephalosporin Pregnant women hospitalized for 2-3 days f/u culture in two weeks

       Stress incontinence—invol. loss of urine w/ activities that increase intraabdominal pressure Urge incontinence—unable to suppress signal from bladder to brain Overflow incontinence-when bladder is distended, will have small amount of incont.

Functional incontinence as seen in Alzheimer’s Reflex incontinence as seen in SCI patients Mixed-stress and urge Neurogenic bladder—lesion of ns leads to urinary incontinence

     May be caused by MS, SCI, HNP, spinal tumor, spina bifida, diabetes Spastic—upper motor neuron lesion Flaccid—lower motor neuron lesion. Fills then have overflow incontinence Assess by checking residuals, I&O, UA, assessing sensory awareness Tx-urecholine, surgery, intermittent caths, S/P caths

        Diuretics CNS depressants which affect LOC CVAs Parkinson’s Depression and altered self-esteem Inability to ambulate safely Assistance products cost prohibitive for patient UTI

   TCAs Anticholinergics—Sudafed, Detrol, Ditropan Estrogen in women

        Weight loss in obese Fluid management Transvaginal or transrectal electrical stimulation Inflatable cuff Vaginal cone retention exercises Urinary catheterization Scheduled toileting Pelvic muscle exercises

   Presence of calculi in urinary tract Cause pain as they pass Nephrolithiasis is formation of stones in the kidney

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Involves three conditions: Slow urine flow resulting in supersaturation of the urine with the particular element Damage to the lining of the urinary tract Decreased inhibitor substances in the urine that would otherwise prevent supersaturation and crystal aggregation

    Metabolic risk factors such as hyperuricemia, hyperoxaluria or hypercalcemia High dietary calcium not contributive unless metabolic or renal tubular defect exists Immobilization Urinary stasis, dehydration and urinary retention mamy be causative

     Evaluate for bladder obstruction UA will reveal RBCs, odor, turbidity, WBCs MRI, KUB, CT Noncontrast helical CT has highest sensitivity IV urography will show obstruction

      Analgesia Avoid NSAIDs if to have lithotripsy (affect platelets) Hydration Urine straining Lithotripsy (monitor ECG and sedate patient) Minimally invasive surgical procedures (MIS) such as stenting, nephrolithotomy

     Antibiotics Thiazide diuretics for hypercalciuria Allopurinol and vitamin B6 for oxalate containing stones Uric acid stone—allopurinol and alkalinizing the urine. Sodium bicarbonate or potassium citrate helpful.

Cystine –captopril and alphamercaptopropionylglycine w/ hydration and alkalinazation of urine

    Urothelial Tx with BCG Radiation chemotherapy

    Ureterostomy Conduits—to intestine and stoma Sigmoidostomies-divert urine to large intestine so no stoma Ileal reservoir—surgically created pouch