Specific Considerations with Renal Disease
Samuel Vanderhoek
William Benedetto
I. GENERAL CONSIDERATIONS
Approximately 5% of the population has renal disease, with a trend toward increasing prevalence with age. Perioperative renal dysfunction complicates patient management and results in increased morbidity and mortality. Aside from optimizing intravascular volume status, there is no definite consensus on prophylaxis for the development of acute kidney injury (AKI). However, morbidity and mortality may be decreased by a thorough understanding of considerations related to renal disease.
II. PHYSIOLOGY
Blood flow to the kidneys is regulated by intrinsic autoregulatory mechanisms, which help maintain volume and composition of body fluids and aid in excretion of metabolites and toxins and retention of nutrients. The kidneys maintain a stable internal balance despite large fluctuations in fluid and solute intake. They regulate intravascular volume, osmolality, acid-base and electrolyte balance, and they excrete hormones as well as the end products of metabolism and drugs.
A. Regulation of Blood Flow
1. The kidneys receive 20% of total cardiac output, with the renal cortex receiving 94% of total blood flow. The renal medulla receives only 6% of total renal blood flow but extracts approximately 80% of the oxygen that it receives, making it very susceptible to ischemia, particularly the medullary thick ascending loop of Henle.
2. Renal blood flow is autoregulated between mean arterial pressures of 60 to 150 mm Hg by intrinsic mechanisms balancing afferent and efferent arteriolar tone. Extrinsic factors such as sympathetic vasoconstrictor innervation, dopaminergic receptors, and the renin-angiotensin system can also alter renal blood flow. Autoregulation can be impaired in states of severe sepsis, AKI, and possibly cardiopulmonary bypass. The kidney is largely devoid of β2-receptors.
B. Fluid Regulation
1. Total body water (TBW) is approximately 60% of body weight. In obese patients, it may be more precise and practical to calculate TBW based on ideal body weight.
a. Two thirds of TBW is intracellular.
b. One third of TBW is extracellular.
1. Two thirds of extracellular fluid is interstitial and one third is
intravascular.
2. Estimated blood volume is 70 mL/kg with an estimated plasma volume of 50 mL/kg.
2. The cells of the macula densa of the thick ascending limb are chemore-ceptors that sense the tubular concentration of sodium and can help to regulate volume status.
3. Hypovolemia is managed by the activation of vasoconstrictor and salt-retaining neurohormonal systems including the following:
a. Renin-angiotensin-aldosterone system
1. The juxtaglomerular apparatus of the kidney secretes renin in response to renal hypoperfusion, decreased sodium chloride delivery to the distal nephron, and increased sympathetic activity. Renin cleaves angiotensinogen to form angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE) in the lung and other tissues.
2. Angiotensin II produces arteriolar vasoconstriction and stimulates aldosterone release.
3. Aldosterone is a mineralocorticoid released by the adrenal cortex in response to angiotensin II, increased potassium levels, decreased sodium content, and adrenocorticotropic hormone. Aldosterone acts on the distal tubules to increase reabsorption of sodium in exchange for potassium and protons.
4. Diuretics abolish the kidneys’ ability to concentrate urine by washing out the renal medullary concentration gradient. Acute tubular necrosis (ATN) presents early as an inability to concentrate urine caused by the breakdown of the Na+/K+-ATPase pump in the medullary thick ascending loop of Henle because of a loss of cell polarity.
b. Arginine vasopressin (AVP) (also called antidiuretic hormone [ADH]) is released by the posterior pituitary gland in response to increased osmolality, decreased extracellular volume, positive pressure ventilation, and surgical stimuli, including pain. AVP increases the permeability of the collecting duct to water through insertion of water channel “aquaporins.” Thus, ADH conserves water and concentrates urine.
4. Hypervolemia
a. Atrial natriuretic peptide, a neuropeptide, is the predominant salt-excreting stimulus along with decreases in angiotensin II and sympathetic activity resulting in decreased sodium resorption, thus producing a dilute urine (300 mOsm/kg) and abundant urine sodium (80 mEq/L). Loop diuretics may produce a similar picture even in the face of hypovolemia.
b. Kinins are converted from kininogens by kallikreins and are regulated by salt intake, renin release, and hormone levels. They cause renal vasodilatation and natriuresis.
5. Osmotic equilibrium
a. The medullary interstitium is kept hypertonic by the countercurrent multiplier effect of the loop of Henle.
b. Calculated osmolality (mOsm/kg) = 2[Na+] + ([blood urea nitrogen] (mg/dL)/2.8) + ([glucose] (mg/dL)/18). Normal osmolality = 290 mOsm/kg.
c. Osmolal gap = Osm (measured) – Osm (calculated) is normally less than 10. An increased osmolal gap occurs when osmotically active but unmeasured substances (e.g., ethanol, mannitol, methanol, and sorbitol) are present in the blood.
6. Daily adult water intake is approximately 2,600 mL: 1,400 mL in liquids, 800 mL in solid food, and 400 mL from metabolism. The minimum water intake to excrete solute load is about 600 mL/day.
C. Electrolyte Balance
1. Disorders of sodium homeostasis
a. Hyponatremia: Plasma sodium concentration less than 134 mEq/L.
1. TBW may be high, low, or normal (usually a sign of free water excess).
2. Hyponatremia often results in reduced plasma osmolality.
3. Pseudohyponatremia from hyperglycemia (uncontrolled diabetes mellitus), hyperlipidemia, or hyperproteinemia (multiple myeloma) should be ruled out to avoid mistreatment.
4. Clinical features vary with the degree of hyponatremia and the rapidity of onset. Symptoms generally do not appear until the sodium concentration falls below 125 mEq/L.
a. Moderate hyponatremia or gradual onset: Confusion, muscle cramps, lethargy, anorexia, and nausea.
b. Severe hyponatremia or rapid onset: Seizures and coma.
5. Generally, acute normalization of the serum [Na+] is not necessary. It should be corrected at a rate of 0.5 mEq/L/h until 120 mEq/L is reached to prevent complications from rapid correction (e.g., cerebral edema, central pontine myelinolysis, and seizures). At this point, the patient should be out of danger, and the [Na+] should be normalized slowly over a period of days. Treatment depends on the volume status of the patient.
a. Hypervolemic hyponatremia due to renal failure, congestive heart failure, cirrhosis, or nephrotic syndrome is treated by sodium and water restriction and possibly with diuresis.
b. Hypovolemic hyponatremia from diuretics, vomiting, or bowel preparations is treated with normal saline. For severe hypovolemic hyponatremia, the [Na+] may be partially corrected to 125 mEq/L or a serum osmolality of 250 mmol/L over 6 to 8 hours with 3.5% hypertonic saline. Hypertonic saline is dangerous in volume-expanded salt-retaining states such as congestive heart failure.
c. Normovolemic hyponatremia from the syndrome of inappropriate ADH secretion, hypothyroidism, drugs that impair renal water excretion, or water intoxication is treated by fluid restriction.
b. Hypernatremia: Plasma sodium concentration greater than 144 mEq/L. It is usually caused by impairment of thirst or the ability to obtain water.
1. TBW may be high, low, or normal (usually a sign of free water deficit).
2. Clinical features vary with the degree of hypernatremia and rapidity of onset, ranging from tremulousness, weakness, irritability, and mental confusion to seizures and coma.
3. Treatment depends on determining the volume status of the patient. Rapid correction can induce cerebral edema, seizures, permanent neurologic damage, and death. Plasma [Na+] should be corrected at a maximum rate of 0.5 mEq/L/h. The water deficit, if present, can be calculated as follows:
Volume to be replaced (L) = [(0.6 × body weight [kg]) × ([Na+] – 140)/140]
a. Hypervolemic hypernatremia occurs secondary to Na+ overload from mineralocorticoid excess, dialysis with hypertonic solutions, or treatment with hypertonic saline or sodium bicarbonate (NaHCO3). The excess total body Na+ (i.e., volume) may be removed by dialysis or with diuretic therapy, and the water loss is replaced with 5% dextrose in water (D5W).
b. Hypovolemic hypernatremia occurs secondary to water loss exceeding Na+ loss (e.g., diarrhea, vomiting, and osmotic diuresis) or inadequate water intake (e.g., impaired thirst mechanism and altered mental status). If hemodynamic instability or
evidence of hypoperfusion is present, initial volume therapy should consist of 0.45% or even 0.9% NaCl. After volume replenishment, the remaining free water deficit should be replaced with D5W until the Na+ concentration decreases. Then, 0.45% saline may be substituted.
evidence of hypoperfusion is present, initial volume therapy should consist of 0.45% or even 0.9% NaCl. After volume replenishment, the remaining free water deficit should be replaced with D5W until the Na+ concentration decreases. Then, 0.45% saline may be substituted.
c. Normovolemic hypernatremia is typically the result of diabetes insipidus in patients with a normal thirst response. Therapy consists of treating the underlying etiology, correcting the free water deficit with D5W, and using exogenous vasopressin in neurogenic diabetes insipidus.
2. Disorders of potassium homeostasis
a. Hypokalemia: Plasma [K+] less than 3.3 mEq/L.
1. Serum [K+] is a poor index of total body potassium stores, because 98% of body potassium is located intracellularly. Thus, large [K+] deficits must be present before seeing a decrease in serum [K+]. In a 70-kg man with normal pH, a fall in serum [K+] from 4 to 3 mEq/L reflects a deficit of 100 to 200 mEq. Below 3 mEq/L, each decrease of 1 mEq/L reflects an additional deficit of 200 to 400 mEq.
2. Etiologies
a. Total body K+ deficit.
b. Shifts in distribution of K+ (extracellular to intracellular).
3. [K+] loss may be from the following:
a. Gastrointestinal tract (e.g., vomiting, diarrhea, nasogastric suctioning, chronic malnutrition, or obstructed ileal loops).
b. Kidney (e.g., diuretics, mineralocorticoid and glucocorticoid excess, and some types of renal tubular acidosis).
4. Changes in K+ distribution occur with alkalosis (H+ shifts to the extracellular fluid and K+ moves intracellularly). Thus, rapid correction of acidosis, by hyperventilation or NaHCO3 administration, may produce undesirable hypokalemia.
5. Clinical features rarely appear unless [K+] is less than 3 mEq/L or the rate of fall is rapid.
a. Signs include weakness, augmentation of neuromuscular block, ileus, and disturbances of cardiac contractility.
b. Hypokalemia increases excitability and predisposes the patient to arrhythmias that may be refractory to treatment unless the hypokalemia is resolved. Electrocardiographic (ECG) changes include flattened T waves, U waves, increased PR and QT intervals, ST segment depression, and atrial and ventricular dysrhythmias. Ventricular ectopy is more likely with concomitant digitalis therapy.
c. Serum [K+] less than 2.0 mEq/L is associated with vasoconstriction and rhabdomyolysis.
6. Treatment. Rapid replacement of K+ may cause more problems than hypokalemia. There is no need to correct chronic hypokalemia ([K+] ≥ 2.5 mEq/L) before induction of anesthesia. Hypokalemia-induced conduction disturbances or diminished contractility can be treated with K+ (0.5 to 1.0 mEq intravenously [IV] every 3 to 5 minutes) until resolution. Serum [K+] must be closely followed during correction.
b. Hyperkalemia: plasma [K+] greater than 4.9 mEq/L.
1. Certain conditions and drugs can worsen hyperkalemia such as catabolic stress, acidosis, nonsteroidal anti-inflammatory drugs (NSAIDs), ACE-I, potassium-sparing diuretics, and β-blockers.
2. Etiologies
a. Decreased excretion (e.g., renal failure and hypoaldosteronism)
b. Extracellular shift (e.g., acidosis, ischemia, rhabdomyolysis, tumor lysis syndrome, and drugs such as succinylcholine). Acidosis increases the serum [K+] by 0.5 mEq for every 0.1 unit decrease in the pH
c. Administration of blood, potassium penicillins, and salt substitutes to renal failure patients
d. Pseudohyperkalemia from a hemolyzed specimen
3. Clinical features are more likely with acute changes than with chronic elevation.
a. Signs and symptoms include muscle weakness, paresthesias, and cardiac conduction abnormalities, which become dangerous as K+ levels approach 7 mEq/L. Bradycardia, ventricular fibrillation, and cardiac arrest may result.
b. Hyperkalemia suppresses electrical conduction. ECG findings include peaked T waves, ST segment depression, prolonged PR interval, loss of the P wave, diminished R-wave amplitude, QRS widening, and prolongation of the QT interval.
4. Treatment depends on the nature of ECG changes and serum levels.
a. ECG changes are treated with slow IV administration of 0.5 to 1.0 g of calcium chloride (CaCl2). The dose may be repeated in 5 minutes if changes persist.
b. Hyperventilation and NaHCO3 administration shifts K+ intracellularly. Between 50 and 100 mEq of NaHCO3 may be given IV over 5 minutes, with a repeated dose in 10 to 15 minutes.
c. Insulin also shifts K+ intracellularly. Regular insulin (10 units) is given IV simultaneously with 25 g of glucose (one ampule of a 50% solution) over 5 minutes. Check the glucose level 30 minutes later to avoid hypoglycemia.
d. The above therapies are short-term measures to decrease [K+] via cellular shifts. Cation exchange resins (sodium polystyrene sulfonate [Kayexalate], 20 to 50 g with sorbitol) given orally or rectally will slowly remove K+ from the body and should be used as soon as possible. Serum [K+] can also be lowered by dialysis.
D. Extrarenal Regulatory and Metabolic Functions
1. Erythropoietin is produced to stimulate red blood cell production. Treatment of patients with exogenous recombinant erythropoietin can prevent the anemia due to chronic kidney disease (CKD) and its sequelae.
2. Vitamin D is converted to its most active form, 1,25-dihydroxy-vitamin D by the kidney.
3. Parathyroid hormone acts on the kidney to conserve calcium, to inhibit phosphate resorption, and to increase conversion of vitamin D by the kidney.
4. Peptides and protein hormones such as insulin are metabolized, accounting for the generally decreased insulin requirements as renal failure progresses.
III. RENAL FAILURE
The definition varies but has been reported as an increase in serum creatinine by 0.5 mg/dL, increase in serum creatinine by 50%, or serum creatinine greater than 2 mg/dL.
A. Acute Kidney Injury. Incidence varies according to etiology, definition, and type of surgery but is 4% to 24% with mortality rates as high as 60% to 90%. Postoperative renal dysfunction is associated with higher incidence of gastrointestinal bleeding, respiratory infection, sepsis, and longer ICU and hospital length of stay.
1. Epidemiology. From 2% to 5% of hospitalized patients; increases with age.
2. Etiology
a. Prerenal. Due to decreased circulating volume (hypovolemia) or a perceived decrease in circulating volume (decreased cardiac output or hypotension). Early correction of the underlying cause usually results in rapid reversal of renal dysfunction, but continued renal hypoperfusion may result in intrinsic renal damage.
b. Intrarenal. The most common cause is ATN due to ischemia (see section III.C). Other intrarenal causes include toxins, acute glomerulonephritis, and interstitial nephritis.
c. Postrenal. Obstructive lesions result in disrupted emptying and can be caused by renal calculi, neurogenic bladder, prostatic disease, or an encroaching tumor. Unilateral obstruction rarely causes AKI.
d. Normotensive ischemic acute kidney injury. A low-perfusion state may arise in the absence of frank hypotension in a patient with “normal” appearing blood pressures. These patients typically have underlying risk factors for renal injury including early sepsis or exposure to nephrotoxic agents such as IV contrast or NSAIDs. Additionally, normotension in a patient with baseline chronic hypertension can actually herald a low-perfusion state.
3. Classification. There are three widely used classification systems for AKI (Table 4.1):
a. The RIFLE criteria classifies three levels of kidney injury (risk, injury, or failure) and two outcomes (loss and end-stage renal disease [ESRD]) based upon (1) a percentage increase in serum creatinine over 7 days or (2) a decrease in urine output (UOP).
b. The AKIN criteria modifies the RIFLE criteria by including absolute increases in serum creatinine and limiting the period of injury to a 48-hour window.
c. The KDIGO criteria fuses the RIFLE and AKIN criteria.
4. Diagnosis. Clinical features occurring late in the course of the disease include hypervolemia due to an impaired ability to excrete water and sodium with resultant hypertension and peripheral edema, potential hypovolemia due to lack of urine concentrating ability, potassium retention, impaired excretion of drugs and toxins, and potential progression to CKD. Results of urine and serum indices can help to distinguish prerenal, intrarenal, and postrenal etiologies (Table 4.2).
5. Prevention. Mainly based on tradition, anecdotes, or extrapolation from animal models. A modest goal is to keep UOP greater than 0.5 mL/kg/h and to avoid hypovolemia, hypoxia or decreased O2 delivery, renovascular constriction, increased renal O2 demand, and maintenance of renal vasodilation and renal tubular blood flow along with attenuation of renal ischemic reperfusion injury.
6. Treatment
a. Medications such as diuretics, dopamine, and fenoldopam can be used to increase UOP, treat hypertension, and manage electrolyte, fluid, and acid-base disturbances but have not been proven to prevent or treat AKI (see sections IV.A and IV.B).
TABLE 4.1 Criteria for Acute Kidney Injury | ||||||||||||||||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| ||||||||||||||||||||||||||||||||||||||||||
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
