Kidney anatomy
The kidneys are responsible for removing wastes from the body, regulating electrolyte balance and blood pressure, and stimulating red blood cell production.
RENAL DISEASES Terms: *aldosterone *antidiuretic hormone *anuria *bacteriuria *clearance *dysuria *frequency *GFR
*hematuria *nocturia *oliguria *proteinuria *pyuria *Valsalva Leak Maneuver Point *vesicoureteral reflux
Test of Urine Specific Gravity: 1. Osmolality
2. Specific gravity
Illustration
Illustration
Kidneys -retroperitoneal organs -120 – 170g -12cm long, 6cm wide and 2.5cm thick -with 8 – 18 pyramids -with 4 -13 minor calyces -with 2 – 3 major calyces -with protective structures: a. Pararenal fat b. Gerota’s fascia c. Perirenal fat d. Renal capsule
Nephron -basic structural and functional unit of the kidney
3 Processes of Urine Formation 1. Glomerular Filtration 2. Tubular Reabsorption 3. Tubular Secretion Renal function begins to decrease at a rate of 1% each year at 30.
C. Acute Pyelonephritis -bacterial infection of the renal pelvis, tubules and interstitial tissue -an ascending infection -predisposing factors: a. vesico-ureteral reflux b. urinary tract obstruction -enlarged kidney -with abscess on the renal capsule and at the corticomedullary junction
SIGNS AND SYMPTOMS: fever and chills
costo-vertebral angle
leucocytosis bacteriuria and pyuria flank pain
tenderness dysuria increase urinary frequency
DIAGNOSIS: UTZ
Nuclear scan
CT scan IVP
Urine Culture and Sensitivity Test
MEDICAL MANAGEMENT: a. uncomplicated -no dehydration, no nausea and vomiting, no sepsis >2 weeks of oral antibiotics Trimethoprim-Sulfamethoxazole Ciprofloxacin Gentamicin with or without Ampicillin Third Generation Cephalosporins >6 weeks of oral antibiotics if with relapse *urine culture 2 weeks after antibiotic therapy b. complicated -pregnant patients >hospitalization (antibiotics from IV to oral)
B. Chronic Pyelonephritis -repeated acute pyelonephritis >> chronic pyelonephritis -no s/sx unless there’s an acute exacerbation -kidneys scarred, contracted and non functional SIGNS AND SYMPTOMS: fatigue headache anorexia
polyuria excessive thirst weight loss
DIAGNOSIS: creatinine and BUN clearance creatinine levels intravenous pyelography
COMLICATIONS: a. ESRD b. hypertension c. formation of renal stones -may be due to the presence of urea splitting microorganisms
MEDICAL MANAGEMENT: a. urine culture and sensitivity guided antibiotic therapy Nitrofurantoin TMP-SMZ
NURSING MANAGEMENT: a. monitoring -I&O b. oral fluids (3-4L/day)
c. symptomatic -antipyretics d. education -advise bed rest -prevention of UTI
C. Acute Glomerulonephritis -primarily a disease of children older than 2 years old -may affect any age -causes: >autoimmune SLE >streptococcal Acute Post Streptococcal Glomerulonephritis
Acute Post Streptococcal Glomerulonephritis -2 to 3 weeks after >impetigo >sorethroat SINGS AND SYMPTOMS: hematuria tea colored urine proteinuria inc serum BUN and crea anemia edema
hypertension headache, malaise, flank pain (+) kidney punch congestion confusion, somnolence and seizures
Group A Beta-Hemolytic Streptococcal Infection Antigen-Antibody Reaction Deposition in the Glomerulus Increased Production of Epithelial Cells in the Glomerulus WBC Infiltration Thickening Scarring Decreased GFR
DIAGNOSIS: a. kidney biopsy b. electron microscopy c. immunoflourescence analysis d. Anti-Streptolysin O Titer Anti-DNAse B Titer e. Serum Complement Determination -decreased -will normalize in 2 – 8 weeks IgA Nephropathy -most common type of primary glomerulonephritis -Inc IgA; with normal serum complement -complications: a. Hypertensive Encephalopathy b. Heart Failure c. Pulmonary Edema
Rapidly Progressive Glomerulonephritis -patient deteriorates in weeks to months -course is more severe and more rapid
Management To Glomerulonephritis Goals: 1. 2. 3.
Treat symptoms Preserve renal function Treat complications a. antibiotics b. steroids c. cytotoxic agents
d. protein restriction e. sodium restriction f. diuretics g. dialysis
D. Chronic Glomerulonephritis -components: repeated acute glomerulonephritis hypertensive nephrosclerosis hyperlipidemia chronic tubulo-interstitial injury hemodynamically mediated glomerular sclerosis -contraction of the kidneys to 1/5 of its original size -deformed kidneys -may result to ESRD SIGNS AND SYMPTOMS: may be asymptomatic hypertension inc BUN and Crea bipedal edema
retinal hemorrhages ophthalmoscopy papilledema weight loss weakness and irritability nocturia GIT disturbances anemia heart failure peripheral neuropathy, decreased DTR pulsus paradosus DIAGNOSIS: 1. Urinalysis- fixed sp. Gravity at 1.010 proteinuria; urinary casts
2. serum chemistry -hyperkalemia - hypoalbuminemia -hyperphosphatemia -hypocalcemia -hypermagnesemia 3. CBC -anemia 4. Chest X-Ray -cardiomegaly -pulmonary edema 5. ECG -left ventricular hypertrophy
MANAGEMENT: 1. 2. 3. 4. 5.
treatment of hypertension weight monitoring give proteins of high biologic value adequate calories dialysis
NURSING MANAGEMENT: 1. monitoring E. Nephrotic Syndrome -components: proteinuria hypoalbuminemia
hyperlipidemia
CAUSES: a. chronic glomerulonephritis b. diabetes mellitus c. amyloidosis d. SLE e. multiple myeloma f. renal vein thrombosis SIGNS AND SYMPTOMS: edema (soft and pitting) -eyes, dependent area and abdomen malaise irritability headache fatigue
DIAGNOSIS: 1. Urinalysis -proteinuria (3-3.5g/day) -inc WBC 2. Protein Electrophoresis Immunoelectrophoresis 3. Biopsy 4. AntiC1q antibodies (SLE)
COMPLICATIONS: a. infection b. thromboembolism atherosclerosis c. pulmonary emboli
d. acute RF e. accelerated
MANAGEMENT: 1. diuretics 2. ACE inhibitors 3. immunosuppressants 4. steroids 5. hypolipidemic agents 6. sodium restriction 7. CHON intake of 0.8g/kg/day low saturated fats
Urolithiasis -stones or calculi in the urinary tract -supersaturation of substances such as calcium oxalate, calcium phosphate and uric acid SIGNS AND SYMPTOMPS: >depends on *the site of obstruction *edema *infection ASSESSMENT AND DIAGNOSIS: >IVP, Intravenous Urography >Retrograde Pyelography >UTZ >serum chemistries and 24 urine tests
deficiency of citrate, mg nephrocalcin & uropontin dehydration infection
Urolithiasis urinary stasis periods of immobility hypercalciuria and hypercalcemia
Causes of hypercalcemia and hypercalciuria:
a. hyperparathyroidism b. renal tubular acidosis c. cancers d. granulomatous disease e. excessive intake of Vitamin D f. excessive intake of milk and alkali g. myeloproliferative disease -substances other than calcium that may precipitate and form stones a. uric acid -5%-10% of renal stones -gout, myeloproliferative disorders
b. struvite -15% of renal stones -in persistently alkaline and ammonia rich urine (caused by urease-splitting bacteria) -in neurogenic bladder, foreign bodies and recurrent UTI
c. cystine -1%-2% of renal stones -hereditary defect in the renal absorption -medicines that increases the risk of urolithiasis a. acetazolamide b. Vitamin D c. antacids
d. laxatives e. high doses of aspirin
MANAGEMENT: a. eradicate the stone b. determine the stone type c. prevent nephron destruction d. control infection e. relieve any obstruction >Opioid Analgesics NSAIDs >Hot Baths and Moist Heat to the flank area >Advise to increase oral fluid intake (urine output of >2L/day is advisable)
SPECIFIC MANAGEMENT: 1. Calcium stones -restrict proteins and sodium in the diet -acidify the urine using Ammonium chloride or Acetohydroxamic Acid -Cellulose sodium phosphate (binds calcium from food) -thiazide diuretics (if caused by inc PTH) 2. Uric Acid Stones -low purine diet (shellfish, mushrooms, asparagus, organ meats) -Allopurinol -alkalinize the urine
3. Cystine -low protein diet -penicillamine (to decrease excretion through the urine) 4. Oxalate -dilute the urine -limit oxalate containing foods (spinach, strawberries, rhubarb, tea, bran)
SURGICAL MANAGEMENT: a. Ureteroscopy b. Extracorporeal Shock Wave Lithotripsy c. Percutaneous Nephrostomy or Nephrolithotomy
ACUTE RENAL FAILURE
A c u t e K i d n e y F a i l u r e
A c u t e K i d n e y F a i l u r e
Acute kidney failure occurs when the kidneys suddenly stop working. This may occur after surgery or due to an injury. It can also occur due to the use of certain drugs. People with acute renal failure may regain their kidney function depending on the cause of the damage.
Acute Renal Failure
-sudden and almost complete loss of renal function -s/sx: *oliguria *normal urine output *anuria *rising serum creatinine and BUN 1. Prerenal -shock 2. Intrarenal -the result of actual parenchymal damage -use of nephrotoxic drugs (NSAIDs and ACE inh) 3. Postrenal -the result of an obstruction in the distal urinary tract
Acute Renal Failure
ACUTE RENAL FAILURE
PRE-RENAL
INTRA-RENAL
POST-RENAL
Four Clinical Phases of ARF 1. Initiation -begins with the initial insult and ends when oliguria develops 2. Oliguria -rise in the serum of waste products of metabolism -rise in serum potassium and magnesium 3. Diuresis -with gradually increasing urine output -renal function may still be markedly abnormal 4. Recovery Period -improvement of renal function -may take 3-12 months -with normal laboratory values -with permanent 1-3% reduction in GFR
Characteristics
Prerenal
Intrarenal
Postrenal
Etiology
hypoperfusion
parenchymal damage
obstruction
BUN value
increased
increased
Increased
Creatinine value
increased
increased
Increased
Urine output
decreased
varies, often decreased
varies, may be decreased or anuria
Urine sodium
Decreased, <20mEq/L
Increased, >40mEq/L
Varies, often <20mEq/L
Urinary Sediment
Normal, few hyaline casts
Abnormal casts Usually normal
Characteristics
Prerenal
Intrarenal
Postrenal
Urine osmolality
Increased to 500mOms
Abnormal casts Usually normal and debris
Urine specific gravity
Increased
Low normal, 1.010
Varies
ASSOCIATED PROBLEMS: *metabolic acidosis *hyperphophatemia and hypocalcemia *anemia
PREVENTION: *prevention of exposure to nephrotoxic drugs -aminoglycosides, cyclosporine, amphotericin B *serum BUN and creatinine monitoring MANAGEMENT: a. restore chemical balance and prevent complications b. identification and treatment of the underlying cause c. maintain fluid balance -BP, CVP, serum and urine elect., fluid loses
d. monitoring for over hydration -dyspnea, crackles, distended neck veins -Furosemide, Ethacrynic Acid e. dialysis -to prevent serious complications *hyperkalemia *severe metabolic acidosis *pericarditis *pulmonary edema f. pharmacologic -cation exchange resin (sodium polystyrene sulfonate-kayexalate)
-retention enema -diuretic therapy -low dopamine dose (1-3g/kg) -phosphate binding agents (AlOH) g. nutritional therapy -give additional proteins (1g/kg/day during the oliguric phase) -high potassium and phosphate foods are restricted (banana, citrus and coffee) -potassium restricted to 20-40mEq/day -sodium restricted to 2g/day -may require parenteral nutrition
NURSING MANAGEMENT: a. monitoring fluid and electrolyte balance b. reducing metabolic rate -bed rest, prevention of fever and infection c. promoting pulmonary function -assistance in changing positions -advise to cough and deep breath d. preventing infection -asepsis -avoid inserting an indwelling urinary catheter e. providing skin care f. providing support
CHRONIC RENAL FAILURE
Patients with kidney dysfunction (i.e. Renal Failure) are typically identified by the increased blood levels of Cr and BUN on routine bloo lab testing. By definition we separat kidney failure into ACUTE vs. CHRONIC.
Chronic Renal Failure -is a progressive irreversible deterioration in renal function -with uremia or azotemia (severity of build up will be proportional to the severity of s/sx) -prognosis will be determined by the presence or absence of hypertension and proteinuria CAUSES: *diabetes mellitus- most common *hypertension *chronic glomerulonephritis *obstruction of the urinary tract *polycystic kidney disease *infections *nephrotoxic medications
STAGES: Stage 1 -Reduced Renal Reserve -40%-75% loss of nephron function -usually asymptomatic Stage 2 -Renal Insufficiency -75%-90% loss of nephron function -increase in serum BUN and creatinine -inability to concentrate urine -anemia may develop -with polyuria and nocturia Stage 3 -End Stage Renal Disease -<10% of nephron function remaining -regulatory, excretory and hormonal functions are lost -requires dialysis
SIGNS AND SYMPTOMS cardiovascular *hypertension *pulmonary edema *heart failure *pericarditis dermatologic *pruritus *uremic frost (deposit of urea crystals) GI and Neurologic s&sx
ASSESSMENT AND DIAGNOSIS: a. glomerular filtration rate creatinine clearance b. serum electrolytes c. ABG d. CBC
COMPLICATIONS: a. Hyperkalemia b. Pericarditis, Pleural Effusion and Cardiac Tamponade c. Hypertension d. Anemia e. Bone Disease
MEDICAL MANAGEMENT: a. maintain kidney function and homeostasis b. treat the underlying cause and contributory factors >medications >dialysis >diet therapy 1. Pharmacologic Therapy a. antihypertensives > includes intravascular volume control *fluid restriction *sodium restriction b. sodium bicarbonate c. erythropoietin >will achieve a Hct of 33%-38%
>IV or SC 3x a week >takes 2-6 weeks to increase Hct >A/R: *hypertension *increased clotting of vascular access sites *seizures *depletion of body iron stores d. iron supplementation e. antiseizure agents >Diazepam >Phenytoin f. antacids
>aluminum based antacids neurologic symptoms osteomalacia >calcium carbonate 2. Nutritional Therapy -regulation of protein intake -regulation of fluid intake (500-600ml more than the previous day’s 24 hour UO) -regulation of sodium intake -regulation of potassium -adequate calories and vitamins 3. Dialysis -to prevent hyperkalemia
NURSING MANAGEMENT: a. avoid the complications of reduced renal function b. assess fluid status c. identify potential sources of the imbalance d. implement a dietary program e. encourage self care and independence
ADPIE Assessment Subjective: Dysuria and Frequent urination Objective: Hyperthermia Urinary incontinence or retention Nursing Diagnosis -Impaired urinary elimination r/t renal problems as evidenced by urinary incontinence. -Hyperthermia r/t kidney infections. -Acute pain r/t damaged kidney.
ADPIE Planning STG: After an hour of nursing intervention the patient’s body temperature will decreased and the pain will be verbalized as tolerable. LTG: Within hospital stay the patient will maintain normal body temperature, verbalizes pain not occurring and will maintain normal urinary elimination. Intervention -TSB -Provide teachings of safety measures -Explain patient’s condition -Monitor VS to know any alteration -Assess patient’s pain tolerance -Administer medications as prescribed -Monitor I and O Evaluation STG: After an hour of nursing intervention the patient’s body temperature has reduced and the patient verbalizes pain as tolerable. LTG: Within hospital stay the patient has maintain normal body temperature, verbalizes pain not occurring and has maintained normal urinary elimination.
REFERENCES
Brunner and Suddarth’s Textbook of Medical and Surgical Nursing 10th Edition, Suzanne C. Smeltzer; Brenda Bare www.google.com
END!!! GoD Bless