Kidney Failure

ACUTE KIDNEY INJURY

Acute kidney injury (AKI) is a condition of abrupt deterioration in renal function as evidenced by rising blood urea nitrogen (BUN) and creatinine and usually decreased urine output. Approximately half of all cases occur in the surgical setting, and early recognition can minimize the extent of renal injury. The following is a brief review of the three major classifications of acute renal failure.

Prerenal

Prerenal azotemia is the direct result of inadequate renal perfusion. If the reason for poor perfusion can be rapidly reversed, resolution of the problem can usually be expected. However, prolonged low-flow states can produce an intrinsic ischemic injury to the kidney (i.e., acute tubular necrosis [ATN]).

▪ Causes of Prerenal Azotemia

Volume depletion (hemorrhage and dehydration)
Low cardiac output (congestive heart failure, cardiogenic shock, and tamponade)
Renal artery (stenosis, occlusion, and vasoconstriction)
Systemic vasodilatation (sepsis, anaphylaxis, and overdose)

Postrenal

Obstruction to urine flow can occur anywhere in the urinary tract. Proximal to the obstruction, pressures within the collecting system and renal tubules will rise. Ultimately, renal injury will result because of cellular atrophy and necrosis if the obstruction to urine flow is not relieved. Recovery of some renal function can generally be expected in cases of complete unilateral ureteral obstruction if flow is restored within 6 weeks.

▪ Causes of Urinary Obstruction

Bladder outlet (benign prostatic hyperplasia, strictures, bladder neck contracture, stones, foreign body, tumor, blood clots, etc.)
Ureters (stones, intrinsic and extrinsic tumors, retroperitoneal fibrosis, papillary necrosis, and ureteropelvic junction obstruction)

Intrarenal

Acute parenchymal kidney injury is the result of tubular cell damage from hypoperfusion, nephrotoxic injury, or an inflammatory process.

▪ Causes of Intrinsic Parenchymal Renal Disease

ATN can be conveniently divided into three phases: (a) onset, (b) oliguric, and (c) postoliguric. The oliguric period (urine output <500 mL/24 hour) typically lasts 10 to 14 days; however, it may be as brief as 2 days or as long as 6 to 8 weeks. A nonoliguric ATN can occur, particularly when secondary to nephrotoxic injury such as aminoglycosides or radiographic contrast agents. Causes of ATN include the following:
- Ischemic injury from renal hypoperfusion (hypotensive episodes, cardiogenic or septic shock, etc.) is the most common cause of ATN in hospitalized patients
- Nephrotoxins (aminoglycosides, anesthetics, iodinated contrast media, and nonsteroidal anti-inflammatory drugs [NSAIDs])
- Hemoglobinuria or myoglobinuria (intravascular hemolysis or rhabdomyolysis)
Acute glomerular nephritis—urinalysis is important (proteinuria, hematuria, and red blood cell casts)
Acute interstitial nephritis—sterile pyuria, white blood cell casts, and eosinophiluria, most often caused by drugs (NSAIDs, sulfonamides, cimetidine, allopurinol, and ciprofloxacin)

Evaluation of Acute Renal Failure

The workup of a patient with sudden elevation of BUN and creatinine with or without decreased urine output requires a prompt, systematic approach to exclude any reversible pathophysiologic
states and remove any potentially nephrotoxic agents. Prerenal and postrenal causes must be excluded before diagnosing intrinsic renal disease.

▪ Renal Hypoperfusion

Evaluate Circulatory System

Measure heart rate, blood pressure, postural hypotension, jugular venous distention, central venous pressures, and cardiac output (Swan-Ganz catheter if necessary) and listen to the chest for evidence of failure.

Check Volume Status

Assess weights, input/output records, skin turgor, mucus membranes, recent surgery, gastrointestinal bleeding, urine specific gravity (usually >1.015-1.020) and/or osmolality, BUN/creatinine ratio (>20:1), spot urine sodium (<5 mEq/L), and fractional excretion of sodium.

Urinalysis

Urinalysis is typically unremarkable.

Evaluate Renal Vasculature

Obtain diethylenetriaminepentaacetate (DTPA) renal scan, arteriography, or venography.

▪ Urinary Obstruction

Bladder outlet

Place a Foley catheter or irrigate existing catheter.

▪ Intrinsic Kidney Injury

Urinalysis

The urinary sediment will typically show renal tubular cell casts during the early stages of ATN. Urine specific gravity is usually fixed at 1.010 to 1.012, and the urinary sodium concentration is >30 to 40 mEq/L. Proteinuria is observed with glomerular disease and to a lesser extent with interstitial disease.

Ischemia

Look for periods of hypotension (e.g., recent surgery or septic or cardiogenic shock).

Nephrotoxins

Carefully check for medications that can cause ATN (e.g., aminoglycoside antibiotics, and recent radiographic contrast studies) or interstitial nephritis (e.g., sulfa drugs, penicillin, furosemide,
hydrochlorothiazide, and dilantin) or medications that exacerbate prerenal azotemia (e.g., prostaglandin inhibitors, NSAIDs).

Hemoglobinuria or Myoglobinuria

Look for recent trauma, burns, or surgery.

Management of Acute Kidney Injury

Reverse any pathophysiologic states—restore volume, support blood pressure, and treat sepsis or cardiac failure.
Relieve any urinary obstruction—ensure adequate drainage of urinary tract as needed (e.g., Foley catheter, suprapubic tube, ureteral stents, and nephrostomy tubes). Monitor and treat postobstructive diuresis.
Remove any nephrotoxic agents; stop any nephrotoxic drugs (i.e., change antibiotics as needed, discontinue NSAIDs).
Restrict sodium, potassium, and fluid intake.
Minimize the risk of infectious complications—avoid the use of Foley catheters or central venous lines if possible.
Convert to nonoliguria if possible—persistent oliguria after correction of pre- and postrenal causes is strong evidence of intrinsic renal failure. A trial of furosemide or an osmotic diuretic may convert the patient from oliguric to nonoliguric renal failure. This will make patient management easier and decrease the frequency and duration of dialysis during the recovery phase.
Support with dialysis as needed.

▪ Indications for Dialysis in Acute Kidney Injury

Volume overload manifested by pulmonary edema and decreased PO₂ unresponsive to diuretics
Hyperkalemia and/or marked acidosis in the setting of volume overload
Uremic manifestations (e.g., change in mental status, seizures, cardiac complications, and gastrointestinal bleeding)
BUN >100 or creatinine >10 without clear prospects for early recovery

CHRONIC KIDNEY DISEASE

Etiology

Chronic kidney disease (CKD) is caused by a spectrum of diseases resulting in progressive irreversible loss of functioning
nephrons, ultimately leading to end-stage renal disease (ESRD) requiring dialysis or transplantation if not halted. The most common etiologies are diabetes mellitus, hypertension, primary and secondary glomerular diseases, hereditary kidney disease, obstructive uropathy, chronic infection, and interstitial nephritis.

Manifestations

Uremic symptoms of CKD rarely occur until the glomerular filtration rate (GFR) is <25 mL/minute (25% of normal) or the serum creatinine level is >3 to 4 mg/dL. A wide variety of systemic symptoms involving all organ systems can be seen. This multisystem involvement can make management of these patients quite difficult.

▪ Metabolic

Hyperphosphatemia

Hyperphosphatemia is an early and cardinal manifestation of ESRD and is in itself responsible for many secondary stigmata of the disease. Some evidence suggests that reducing dietary phosphate intake can slow progression of CKD.

Hyperkalemia

Hyperkalemia is generally not a problem in CKD until the GFR drops below 5 mL/minute.

Acidosis

A positive anion gap metabolic acidosis occurs because of the impaired ability of the kidneys to produce ammonia (if GFR is <25 mL/minute).

▪ Gastrointestinal

Gastrointestinal involvement includes nausea, vomiting, anorexia, a metallic taste, uremic stomatitis, glossitis, esophagitis, gastritis, peptic ulcer disease from gastric hypersecretion, colitis, diverticulosis, constipation, and fecal impaction. Upper and lower gastrointestinal bleeding are not uncommon complications.

▪ Hematologic

A normochromic normocytic anemia secondary to marrow suppression and decreased renal erythropoietin occurs when the BUN exceeds 60 to 80 mg/dL or the creatinine level increases above 2 to 3 mg/dL. Thrombocytopenia and platelet
dysfunction also occur. Patients undergoing surgery (especially transurethral resection of the prostate) are at increased risk for bleeding complications. Dialysis helps to partially reverse these problems.

▪ Neurologic

Uremic peripheral neuropathy and encephalopathy can be controlled with adequate dialysis or transplantation.

▪ Cardiovascular

CKD is associated with an increased incidence and severity of atherosclerosis. Derangements in protein and lipid metabolism with hypertriglyceridemia and prolonged hypertension are considered to be major factors involved.

▪ Endocrine Dysfunction

Renal Osteodystrophy

The abnormal bone metabolism found in CKD has a multifactorial origin. First, hyperphosphatemia, due to reduced GFR, directly lowers serum ionized calcium. This reduction stimulates parathyroid hormone secretion (secondary hyperparathyroidism) and consequent bone resorption. Second, loss of renal parenchyma results in decreased renal conversion of 25-hydroxy-D₃ to the active 1,25-dihydroxy-D₃

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