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R. Reti, D. Findlay (eds.)Oral Board Review for Oral and Maxillofacial Surgeryhttps://doi.org/10.1007/978-3-030-48880-2_15
15. Renal Disease
Acute renal failureAzotemiaHemodialysisAcute kidney injury (AKI)Chronic kidney disease (CKD)End stage renal disease (ESRD)Uremia
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The kidney has metabolic and synthetic functions [1, 2]. The metabolic functions take place via a balance of filtration, reabsorption, and secretion.
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The functions of the kidney include the following:
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Elimination of metabolic waste and non-essential materials.
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Fluid balance, electrolyte balance, and composition.
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Maintenance of acid/base levels.
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Secretion of renin by the juxtaglomerular cells.
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Secretion of erythropoietin, conversion of vitamin D, calcium and phosphorus homeostasis.
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Regulation of blood pressure.
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Renal function is measured by the glomerular filtration rate (GFR).
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GFR is estimated using the Cockroft-Gault formula = [(140−age) × (lean body weight in kg) × (0.85 if female)/(serum creatinine mg/dL) × 72].
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GFR is expressed per 1.73 m2 surface area; affected by age, sex, and body size.
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Average GFR for adult male = 130 mL/min [3].
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Average GFR for adult female = 120 mL/min [3].
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Chronic kidney disease occurs when GFR is reduced by at least 50 mL/min or when it is lower than 60 mL/min/1.73 m2 [3].
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GFR is most commonly measured using the body’s clearance of the creatinine; creatinine is a by-product of muscle metabolism; it is almost exclusively filtered through the glomeruli of the kidney, therefore, making it a good clinical indicator of renal function.
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Stages of Renal Dysfunction and Failure
Acute Renal Failure (ARF)/Acute Kidney Injury (AKI)
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The loss of renal function over hours to days that results in disturbances in fluid, electrolyte, and acid-base homeostasis. Diagnosis is based upon a serum creatinine increase by more than 0.5 mg/dL or a serum creatinine concentration rise of more than 25% in a patient with chronic kidney disease and a reduction of GFR by 50% [4].
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This is most commonly measured using creatinine levels as it approximates GFR closely.
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Blood urea nitrogen (BUN) levels are also helpful, but less reliable due to other distracting factors (e.g., GI bleeding, increased protein intake, low urine output/dehydration, use of catabolic drugs such as steroids and tetracycline) as they can cause false elevation [3]. Also, up to 50% of BUN can be reabsorbed, while a negligible amount of creatinine is secreted.
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The most accurate estimate of renal function is a 24-hour urine collection, which is used to compare differences in plasma to urine creatinine and nitrogen levels.
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ARF is classified into three categories (Table 15.1) [3, 4]:
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Prerenal azotemia – conditions that cause a fall in GFR because of reduced glomerular perfusion pressure (BUN:CR > 20:1 and a FENA < 1%).
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Intrinsic renal failure – direct damage to the structures of the kidney.
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Post renal failure – obstruction from either upper or lower urinary tract.
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Causes of AKI
|
Pre-renal (60%) |
Renal (intrinsic) (30%) |
Post-renal (obstructive) (10%) |
|---|---|---|
|
Hypovolemia – decreased renal perfusion: hemorrhage, diarrhea, diuretics Hypotension/reduce blood flow: cardiac failure, sepsis, dehydration Drugs: ACE inhibitors, NSAIDs (altering PG and ATII levels that maintain renal perfusion) Intraoperative: stimulation of renin-angiotensin-aldosterone axis causes vasoconstriction Postoperative: intravascular volume depletion (redistribution of ECF, CHF, MI, vascular obstruction) |
Acute tubular necrosis (ATN) – Injury that directly damages the tubular epithelial cells Common causes are toxic, septic and ischemic Toxins: ethylene glycol, contrast dye, myoglobinuria, NSAIDS, aminoglycosides and amphotericin B Ischemia: embolism, dissection, cardiovascular surgery, severe blood loss, and severe hypotension Sepsis Acute interstitial nephritis (AIN) – edema and inflammation of the renal interstitium Drugs implicated in AIN: penicillin, diuretics, cimetidine, NSAIDs |
Renal vein occlusion Urinary tract obstruction Anticholinergic-associated bladder dysfunction from anesthetic agents or antihistamines |
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Detailed history and physical including pertinent labs (CBC with differential, CMP, coagulation profile, urinalysis, urine electrolytes).
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FENa = fractional excretion of sodium in urine; measures the differences between sodium and creatinine in the plasma (P) and urine (U); (U Na/P Na)/(U Cr/P Cr) × 100%.
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Clinical signs include the following:
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Patient may or may not be oliguric (<400 mL/d) or anuric (<50 mL/d).
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Volume depletion: orthostatic hypotension, tachycardia, dry mucous membranes.
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Dermatologic signs: rash, purpura, livedo reticularis (mottled reticular lace-like purplish skin discoloration caused by capillary obstruction), gangrene, digital cyanosis (AIN or renal artery occlusion) [3].
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Cardiovascular signs: third heart sound, jugular venous distension, and peripheral and pulmonary edema (cardiac failure).
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Upper quadrant tenderness (ureteral obstruction or renal infarction).
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Laboratory findings of acute renal failure (Table 15.2).
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Urinalysis findings in ARF:
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Brown granular casts and epithelial cells represent ischemia or nephrotoxic ARF.
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Heme in the absence of red blood cells represents rhabdomyolysis.
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Eosinophils associated with fever, rash, peripheral eosinophilia represent AIN.
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Red cells casts, protein, red blood cells represent glomerulonephritis.
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Laboratory findings in acute renal failure
|
Pre-renal |
Renal |
Post-renal |
|---|---|---|
|
Urinalysis normal BUN:CR ratio 20:1 (characteristic) Urinary Na < 20 mEq/L Urine osmolality >500 mOsm/kg FENa < 1% |
Urinalysis abnormal and BUN:Cr ratio normal Urinary Na > 40 mEq/L Urine osmolality <350 mOsm/kg |
Normal urinalysis BUN:Cr ratio elevated FENa > 1% |
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Preoperative hypotension and volume depletion can lead to perioperative renal ischemia and, therefore, the aforementioned must be addressed prior to surgery.
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Identify potential risk factors: volume depletion, hypotension, sepsis, nephrotoxic exposure, preexisting chronic kidney disease.
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Elective surgery should be postponed until abnormalities have improved.
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Discontinue or use NSAIDs cautiously. NSAIDs inhibit the synthesis of prostaglandins, which are vital in the maintenance of renal blood flow and GFR. This puts the kidney at risk for perioperative failure in the susceptible patient.
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Consider short-term discontinuation of ACE inhibitors and angiotensin receptor blockers (ARBs). These inhibit actions on the efferent arterioles and worsen ARF [3].
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Avoid radiocontrast (RC) dye in patients with elevated BUN/Cr or chronic renal insufficiency. RC dye can cause direct toxic effects on the kidney or alter the production of nitrous oxide leading to acute failure [3]. Consider pre-treatment with N-acetylcysteine or sodium bicarbonate, which are protective agents; always minimize contrast loads and administer post-procedure hydration.
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Treat underlying cause postoperative ARF [3]:
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Identify and eliminate causative agents.
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Aggressive hydration.
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Eliminate all nephrotoxins.
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If obstructive, relieve obstruction.
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Dialysis is the last resort if there is fluid overload, significant electrolyte abnormalities, and acid–base imbalances that are not relieved by the preceding measures.
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