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.

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.

1. Hypertension2. Diabetes mellitus3. Immobilization4. Parkinson’s disease5. SLE6. Gout7. Sickle cell anemia, multiple myeloma8. BPH9. Pregnancy10. 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

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

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

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

1. Initiation occurs with the insult2. Oliguria with urinary output less than

400ml/24h . rising potassium, BUN, Cr. Not responsive to fluid challenges.

3. Diuresis period— gradual increase in urinary output. Beginning recovery. Renal function gradually improves

4. 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

1. GFR greater than or equal to 90mL/min/1.73 m2. Kidney damage w/normal or increased GFR

2. GFR = 60-89, mild decrease in GFR3. GFR = 30-59, moderate decrease in GFR4. GFR = 15-29. severe decrease in GFR5. 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

Indications:1. Uremia2. Persistent hyperkalemia3. Uncompensated metabolic acidosis4. Fluid volume excess5. Uremic encephalopathy6. 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, 3rd 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

Involves three conditions:1. Slow urine flow resulting in

supersaturation of the urine with the particular element

2. Damage to the lining of the urinary tract3. 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