A review:RENAL PHYSIOLOGY Ma. Tosca Cybil A. Torres, RN
Structure of the kidney• Specific components are nephrons, collecting ducts and a unique microvasculature• Multipapillary kidney of humans – 1 million nephrons• This number already established prenatally – Lost nephrons cannot be replaced
Nephrons• A renal corpuscle (glomerulus) – A knot of capillaries – Connected to a complicated and twisted tubule – Finally drains into a collecting duct
Renal physiology• Prime function – to maintain a stable milieu interieur – By selective retention and elimination of • Water • Electrolytes • And other solutes
Contribution of different nephron segments to solute and water hemostasis (1)• Glomerulus – forms an ultrafiltrate of plasma• Proximal tubule – Reabsorbs 65-70% of filtered NaCl and water – Reabsorbs 90% of bicarbonate – Major site of ammonia production – Reabsorbs almost all of glucose and amino acids – Reabsorbs K, phosphate, calcium, magnesium, urea, and uric acid – Secretes organic anions (urate) and cations
Contribution of different nephron segments to solute and water hemostasis (2)• Loop of Henle – Reabsorbs 15-25% of filtered NaCl – Major site of active regulation of Mg excretion• Distal tubule – Reabsorbs a small fraction of filtered NaCl – Major site of active regulation of calcium excretion
Contribution of different nephron segments to solute and water hemostasis (3)• Connecting segment and cortical collecting tubule – Principal cells reabsorb Na and Cl and secret K – Intercalated cells secrete H, reabsorb K and in metabolic alkalosis – secrete HCO3 – Reabsorb water in presence of ADH
Contribution of different nephronsegments to solute and waterhemostasis (4)• Medullary collecting tubule – Site of final modification of urine – Reabsorb NaCl – Reabsorb water and urea relative to amount of ADH present – Secrete H, and NH3 – Contribute to K balance by reabsorption or secretion of K
ANTIDIURETIC HORMONE REGULATION MECHANISMS Osmoreceptors in ↑Osmolarity hypothalamus Hypothalamus↓Blood Volume receptor ↓ ↑ADH Kidneyvolume Atria and great veins tubulesor ↓BP Posterior pituitary gland ↑H2O reabsorption Narcotics, Stress, Anesthetic agents, Heat, ↑vascular Nicotine, Antineoplastic volume and agents, Surgery ↓osmolarity
ALDOSTERONE-RENIN-ANGIOTENSIN SYSTEM Juxtaglomerular RENIN Angiotensinogen in↓Serum Sodium↓Blood volume cells-kidney plasma Angiotensin I Angiotensin- converting enzyme Via vasoconstriction of arterial smooth muscle ↑Sodium Angiotensin II resorption Kidney tubules ALDOSTERONE(H2O resorbed with sodium); Adrenal ↑ Blood Cortex volume Intestine, sweat glands, Salivary glands
REGULATION OF BODY COMPONENTS • Osmosis – Fluid shift from the region of low solute concentration to the region of high solute concentration until the solutions are of equal concentration. – Tonicity is the ability of the solutes to cause as osmotic driving force that promotes water movement from one compartment to another. • Diffusion – The natural tendency of a substance to move from an area of a higher concentration to one lower concentration. It occurs through a random movement of ions and molecules. Ex. exchange of the oxygen and the carbon dioxide Rate of Diffusion Varies Accdg. To: Size of the molecules Concentration of the solution Temperature of the solution
• Filtration – Hydrostatic pressure in the capillaries tends to filter fluid out of the vascular compartment to the interstitial fluid. Movement of water and solutes occurs from an area of high hydrostatic pressure from an area of a lower hydrostatic pressure. – Hydrostatic pressure- pressure exerted by a fluid within a closed system on the walls of a container in which it is contained.
RENALFAILUREMa. Tosca Cybil A. Torres, RN
RENAL FAILURE • Results when the kidneys cannot remove the body’s metabolic wastes or perform their regulatory functions. The substances normally eliminated in the urine accumulate in the body fluids as a result of impaired renal excretion, leading to a disruption in endocrine and metabolic functions as well as fluid, electrolyte, and acid-base disturbances. • It is a systemic disease and is a final common pathway of many different kidney and urinary tract diseases
ACUTE RENAL FAILURE Is a reversible clinical syndrome where there is a sudden and almost complete loss of kidney function (decreased GFR) over a period of hours to days with failure to excrete nitrogenous waste products and to maintain fluid and electrolyte homeostasis. ARF manifests as an increase in serum creatinine (M=53-132umol/L; F=44- 97umol/L) and BUN (7-20mg/dl). Urine volume may be normal, or changes may occur. Possible changes include oliguria (<400ml/day), nonoliguria (>400ml/day), or anuria (<50 ml/day)
Categories of Acute Renal Failure 1. Prerenal- occurs in 60%-70% of cases, is the result of impaired blood flow to that leads to hypoperfusion of the kidney and a decrease in the GFR. Common clinical conditions are volume-depletion states (hemorrhage or GI losses), impaired cardiac performance (MI, HF, or cardiogenic shock), and vasodilation (sepsis or anaphylaxis)
2. Intrarenal- is the result of actual parenchymal damage to glomeruli or kidney tubules. Nephrotoxic agents such as aminoglycosides and radiocontrast agents account for 30% of cases of acute tubular necrosis (ATN), and ischemia due to decreased renal perfusion accounts for more than 50% of cases Characteristics of ATN are intratubular back leak (abnormal absorption of filtrate and decreased urine flow through the tubule), vasoconstriction, and changes in glomerular permeability. These processes result in a decrease of GFR, progressive azotemia, and impaired fluid and electrolyte balance. Conditions such as burns, infections, crush injuries, and severe blood transfusion reactions can lead to intrarenal ARF and ultimately ATN With burns and crush injuries, myoglobin (a CHON released from muscle when injury occurs) and hemoglobin are liberated, causing obstruction, renal toxicity, and ischemia Medications such as NSAIDs and ACE inhibitors interfere with the normal auto regulatory mechanisms of the kidneys and may cause hypoperfusion and eventual ischemia.
3. Postrenal – is usually the result of an obstruction somewhere distal to the kidneys. Pressure rises in the kidney tubules and eventually, the GFR decreases
Comparing Categories of Acute Renal FailureCharacteristics Categories Prerenal Intrarenal PostrenalEtiology Hypoperfusion Parenchymal Obstruction damageBUN value Increased Increased increasedCreatinine Increased Increased IncreasedUrine output Decreased Varies, often Varies, may be decreased decreased, or sudden anuriaUrine sodium Decreased to < 20 Increased to Varies, often mEq/L >40mEq/L decreased to 20mEq/L or lessUrinary sediment Normal, few hyaline Abnormal casts Usually normal casts and debrisUrine osmolality Increased to About 350 mOsm Varies, increased 500mOsm similar to serum or equal to serumUrine specific Increased Low normal Variesgravity
Causes of Acute Renal Failure A. Prerenal 1. Volume depletion resulting from: a. hemorrhage b. renal losses (diuretics) c. GI losses (vomiting, diarrhea, NG suctioning) 2. Impaired cardiac efficiency resulting from: a. MI b. Heart failure c. Dysrhythmias d. Cardiogenic shock 3. Vasodilation resulting from: a. sepsis b. anaphylaxis c. antihypertensive medications or other medications that cause vasodilation
Causes of Acute Renal Failure B. Intrarenal 1. Prolonged renal ischemia resulting from: a. pigment nephropathy (associated with the breakdown of blood cells containing pigments that in turn occlude kidney structures) b. Myoglobinuria (trauma, crush injury, burns) c. Hemoglobinuria (transfusion reaction, hemolytic anemia) 2. Nephrotoxic agents such as: a. Aminoglycosides antibiotics (gentamicin, tobramycin) b. Radiopaque contrast media c. Heavy metals (lead, mercury) d. Solvents and chemicals (carbon tetrachloride, arsenic) e. NSAIDs, ACE inhibitors 3. Infectious processes such as: a. acute pyelonephritis b. acute GN
Causes of Acute Renal Failure C. Postrenal 1. Urinary tract obstruction, including: a. calculi (stones) b. tumors c. BPH d. Strictures e. Blood clots
Phases of ARF 1. Initiation – begins with the initial insult and ends when oliguria develops 2. The oliguria period is accompanied by an increase in the serum concentration of substances usually excreted by the kidneys (uric acid, urea, creatinine, organic acids). In this phase uremic symptoms first appear and life-threatening conditions such as hyperkalemia develop. 3. The diuresis period is marked by a gradual increase in urine output, which signals that glomerular filtration has started to recover. 4. The recovery period signals the improvement of renal function and may take 3-12 months. Lab values return to normal level. Although a permanent 1%-3% reduction in the GFR is common.
Preventing ARF 1. Provide adequate hydration to patients at risk of dehydration: a. surgical patients before, during and after surgery. b. Patients undergoing intensive diagnostic studies requiring fluid restrictions and contrast agents c. Patients with neoplastic disorders of metabolism and those receiving chemotherapy 2. Prevent and treat shock promptly with blood and fluid replacement. 3. Monitor CV and arterial pressures and hourly urine output of critically ill patients to detect the onset of renal failure as early as possible. 4. Treat hypotension promptly. 5. Continually assess renal function when appropriate.
Preventing ARF 6. Take precautions to ensure that the appropriate blood is administered to the correct patient in order to avoid severe transfusion reactions, which can precipitate renal failure. 7. Prevent and treat infections promptly. Infections can produce progressive renal damage. 8. Pay special attention to wounds, burns and other precursors of sepsis 9. To prevent infections from ascending in the urinary tract, give meticulous care to patients with indwelling catheters. Remove catheter ASAP. 10. To prevent toxic drug effects, closely monitor dosage, duration of use, and blood levels of all medications metabolized or excreted by the kidneys.
Medical Management: 1. Pharmacologic therapy a. hyperkalemia is the most life-threatening of the F/E changes that occur in RF, the elevated K levels may be reduced by administering cation-exchange resins (sodium polystyrene sulfonate [Kayexalate] orally or by retention enema. It works by exchanging sodium ions for potassium ions in the intestinal tract. b. Sorbitol may be administered in combination with Kayexalate to induce diarrhea type effect (induce water loss in the GIT) c. If hemodynamically unstable, IV dextrose 50%,insulin and calcium replacement may be administered to shift potassium back into the cells. d. Diuretics are often administered to control fluid volume, but they have not been shown to hasten the recovery form ARF.
Medical Management2. Nutritional Therapy a. Dietary proteins are individualized to provide the maximum benefit. Caloric requirements are met with high-carbohydrate meals, because carbohydrates have a protein- sparing effect. b. Foods and fluids containing potassium or phosphorous such as banana, citrus fruits and juices, coffee are restricted
Nursing Management• Monitoring fluid and electrolyte balance• Reducing metabolic rate• Promoting pulmonary function• Preventing infection• Providing skin care• Providing support
CHRONIC RENAL FAILURE/END STAGERENAL DISEASE (ESRD) Is a progressive, irreversible deterioration in renal function in which the body’s ability to maintain metabolic and fluid and electrolyte balance fails, resulting in uremia and azotemia.
ESRD Causes: 1. DM, HPN, chronic glomerulonephritis, pyelonephritis, obstruction of the urinary tract, hereditary lesions as in polycystic kidney disease, vascular disorders, infections, medications, or toxic agents. 2. Environmental and occupational agents that have been implicated in CRF include lead, mercury and chromium. Dialysis or kidney transplantation eventually becomes necessary for patient’s survival.
Pathophysiology As renal function declines, the end products of CHON metabolism (which are normally excreted in urine) accumulate in the blood. Uremia develops and adversely affects every system in the body. Stages of CRF: are based on the GFR. The normal GFR is 125cc/min/1.73m2 1. Stage 1 = GFR > 90 ml/min/1.73m2. Kidney damage with normal or increased GFR. 2. Stage 2 = GFR = 60-89 mL/min/1.73m2. Mild decrease in GFR. 3. Stage 3 = GFR = 30-59 mL/min/1.73m2. Moderate decrease in GFR. 4. Stage 4 = GFR = 15-29 mL/min/1.73m2. Severe decrease in GFR. 5. Stage 5 = GFR <15 mL/min/1.73 m2. Kidney failure
Clinical Manifestations 1. CV manifestations: a. HPN – due to Na and H20 retention or from R-A-A activation, b. heart failure and edema - due to fluid overload c. pericarditis - due to irritation of pericardial lining by uremic toxins 2. Dermatologic manifestations a. severe pruritus is common b. uremic frost, the deposit of urea crystals on the skin. 3. GI manifestations: a. anorexia, nausea and vomiting, and hiccups b. The patient’s breath may have the odor of urine (uremic fetor); this may be associated with inadequate dialysis 4. Neurologic manifestations a. altered LOC, inability to concentrate, muscle twitching, agitation, confusion and seizures. b. Peripheral neuropathy, a disorder of the peripheral NS, is present in some patients
Assessment and Diagnostic Findings 1. GFR 2. Sodium and water retention 3. acidosis – due to inability of the kidneys to excrete increased load of acid 4. Anemia 5. calcium and phosphorous imbalance – hypocalcemia and increase in phosphorous
Complications 1. Hyperkalemia due to decreased excretion, metabolic acidosis, catabolism and excessive intake (diet, meds and fluids) 2. Pericarditis, pericardial effusion and pericardial tamponade due to retention of uremic waste products and inadequate dialysis. 3. Hypertension due to sodium and water retention and malfunction of the R-A-A system 4. Anemia due to decreased erythropoietin production, decreased RBC life span, bleeding in the GIT from irritating toxins and ulcer formation, and blood loss during hemodialysis 5. Bone disease and metastatic and vascular calcifications due to retention of phosphorous, low serum calcium levels, abnormal vitamin D metabolism and elevated aluminum levels.
Medical Management1. Pharmacologic Therapy a. calcium carbonate (Os-cal) or calcium acetate (Phoslo) are prescribed to treat hyperphosphatemia and hypocalcemia b. Antiseizure agents – diazepam (Valium) or phenytoin (Dilantin) c. Antihypertensive and CV drugs - digoxin (Lanoxin) and dobutamine (Dobutrex) d. Erythropoietin (Epogen) to treat anemia. It is initiated to reach a hematocrit of 33% - 385 and a target hemoglobin of 12g/dl.2. Nutritional Therapy a. low sodium, low CHON and low K diet3. Dialysis
Nursing ManagementNursing Management:1. Assessing fluid status and identifying potential sources of imbalance.2. implementing a dietary program to ensure proper nutritional intake3. promoting positive feelings by encouraging increased self-care and greater independence.4. Provide explanations and information to the patient and family concerning ESRD, treatment options and potential complications.5. Provide emotional support to the patient and family.
DIALYSIS Is used to substitute some kidney functions during renal failure. It is used to remove fluid and uremic waste products from the body when the kidneys are unable to do so. It may be indicated to treat patients with edema that do not respond to treatment. Acute dialysis is indicated when there is a high and increasing level of serum potassium, fluid overload, or impending pulmonary edema, increasing acidosis, pericarditis and severe confusion. It may also be used to certain medications or other toxins in the blood.
DIALYSIS Chronic or maintenance dialysis is indicated in ESRD in the following instances: 1.Presence of uremic signs and symptoms affecting all body systems (nausea and vomiting, severe anorexia, increasing lethargy, mental confusion) 2.Hyperkalemia and fluid overload not responsive to diuretics and fluid restriction. 3.General lack of well-being. An urgent indication for dialysis in patients with CRF is pericardial friction rub.
PERITONEAL DIALYSIS • Indwelling catheter is implanted into the peritoneum. • A connecting tube is attached to the external end of peritoneal catheter T –tube. • Plastic bag of dialysate solution is inserted to the end of T-tube; the other end is recap. • Dialysate bag is raised to shoulder level and infused by gravity in the peritoneal cavity • Infusion time = 10 minutes/2 liters; dwelling time is 4-6 hours depending on doctor’s order. • At the end of dwelling time, dialysis fluid is drained from the peritoneal cavity by gravity • Draining time is 10-20 minutes/2 liters • Then repeat the procedure when necessary
Peritoneal Dialysis• Usually for patients with absolutely no other options of dialysis• Or as a temporary measure until options of dialysis sorted out
Pre and post operative care forTenckhoff catheter insertion• Pre operative care – Fast for 8 hours – Allow essential medications – Bowel preparation not necessary – Removal of body hair limited to that necessary to facilitate performance of procedure – Empty bladder – Single dose of prophylactic antibiotic – Operating room or well equipped procedure room
Pre and post operative care for Tenckhoff catheter insertion • Post operative care – Catheter irrigation with 1 L of heparinized saline performed as an in-and-out flush within 72 hours following surgery and weekly thereafter until PD initiated – Delay PD for a min of 2 weeks to allow wound healing – Change dressings weekly for 2 weeks – Then patient should begin a routine of daily exit-site cleansing with antibacterial soap – Showering only permitted after 1 month if wound healing uncomplicated – Avoid catheter movement at the exit site – Use sterile gauze dressing over exit site – No tub bathing and swimming
PERITONEAL DIALYSIS NURSING CONSIDERATIONS: 1. Dialysate must be room-warmed before use ( for better absorption) 2. Drugs (heparin, potassium and antibiotics) must be added in advance. 3. Allow the solution to remain in the peritoneal cavity for the prescribed time. 4. Check outflow for cloudiness, blood and fibrin (early peritonitis). 5. NEVER PUSH THE CATHETER IN. 6. Monitor the VS regularly. 7. Keep a record of patient’s fluid balance (daily weighing) 8. Monitor blood chemistry 9. Turn the patient side to side if drainage stop 10.Observe for abdominal pain (cold solution), dialysate leakage (prevent infection) 11.Intake must be equal to output.
HEMODIALYSIS Is the process of cleansing the blood of accumulated waste products Patient’s access is prepared and cannulated surgically One needle is inserted to the artery (brachial) then blood flow is directed to dialyzer (dialysis machine) The machine is equipped with semi-permeable membrane surrounded with dialysis solution Waste products in the blood move to the dialysis solution passing through the membrane by means of diffusion Excess water is also removed from the blood by way of ultrafiltration The blood is then returned to the vein after it has been cleansed.
HEMODIALYSIS NURSING CONSIDERATIONS: 1. Blood can be heparinized unless it is contraindicated to prevent blood clot. 2. Dialysis solution has some electrolytes and acetate and HCO3 added to achieve proper pH balance. 3. Methods of circulatory access: AV fistula; AV graft or U-tube 4. Assess the access site for bruit, signs of infections and ischemia of the hand. 5. Absence of thrill may indicate occlusion 6. No BP taking on the access site. 7. Cover the access site with adhesive bandage 8. Dietary adjustments of CHON, Na and fluid intake. 9. Monitor VS regularly 10.Check blood chemistry 11.Constant monitoring of hemodynamic status, electrolytes and acid-base balance.
KIDNEY TRANSPLANT Indicated for ESRD TYPES OF DONOR 1.Living 2.Cadaveric Rejection and infection remain the major complication after surgery. T and B lymphocytes are involved in the rejection response To reduce the rejection process, immunosuppressive drugs are given Watchout for infection after immunosuppressive medications
KIDNEYTRANSPLANT REJECTION RESPONSE 1. Hyper acute – occurs in the OR, kidney turns blue and flabby. Treatment: remove the kidney 2. Accelerated Acute – occurs 48-72 hours post-op; abrupt oliguria is seen. Treatment: dialysis, steroid and immunsuppressive drugs are initiated; with poor prognosis. 3. Acute – occurs 1 week to several weeks post-op, weight gain, oliguria, HPN, increased BUN, enlarged kidney are seen. Treatment: same with accelerated acute; with good prognosis. 4. Chronic – occurs months to years post-op, progressive decreased renal function is seen. Treatment: same as above; poor prognosis.