Renal Disorders

A urinary tract infection may be classified as a catheter-associated urinary tract infection if the patient has been catheterized within the past 48 hr (Talley & Langley, 2021, p. 634).

CAUTIs are caused by a biofilm, a layer of uropathogens living along the catheter, and the best prevention strategy is to avoid catheterization when possible and to remove urinary catheters as soon as they are no longer medically necessary (Talley & Langley, 2021, p. 634).

Choice b is wrong because more than 100,000 colonies of one or more bacterial species in two consecutive urine samples for women, without urinary tract symptoms, describes asymptomatic bacteriuria rather than the criterion that defines a CAUTI (Talley & Langley, 2021, p. 634).

Choice c is wrong because catheters that have been in place longer than 7 days should be considered for removal or replacement before treatment is initiated; duration beyond 7 days is a management consideration rather than the defining criterion (Talley & Langley, 2021, p. 641).

Choice d is wrong because fever with flank pain and costovertebral-angle tenderness describes an upper urinary tract infection such as pyelonephritis, not the definition of a CAUTI (Talley & Langley, 2021, pp. 634, 637).

An elective knee arthroplasty is not an invasive genitourinary procedure, and routine screening for asymptomatic bacteriuria is not indicated except in women who are pregnant, those undergoing invasive genitourinary procedures, or renal transplant recipients (Talley & Langley, 2021, p. 637).

Choice a is wrong because diabetes mellitus is a risk factor for urinary tract infection in both genders, but it is not an indication for screening asymptomatic bacteriuria (Talley & Langley, 2021, pp. 636–637).

Choice c is wrong because age alone does not justify screening; although urinary tract infections are the most common bacterial infection in the elderly, routine screening for asymptomatic bacteriuria is not recommended on the basis of age (Talley & Langley, 2021, pp. 637, 643).

Choice d is wrong because a personal or first-degree family history of urinary tract infection is a contributing factor in women rather than an indication for screening asymptomatic bacteriuria (Talley & Langley, 2021, pp. 636–637).

For uncomplicated cystitis in women, first-line therapy includes fosfomycin 3 g PO as a single dose; nitrofurantoin monohydrate/macrocrystal (Macrobid) 100 mg PO BID for 5 days; and a 3-day regimen, which is preferred over a single-dose regimen because of high relapse rates (Talley & Langley, 2021, pp. 638–639).

Choice a is wrong because fluoroquinolones should be used only when no other alternative is available (Talley & Langley, 2021, p. 639).

Choice b is wrong because trimethoprim-sulfamethoxazole (Bactrim DS) 160 mg/800 mg PO BID is a first-line agent for uncomplicated cystitis when given for 3 days, not 14 days; a 14-day course is used for pyelonephritis (Talley & Langley, 2021, pp. 639–640).

Choice d is wrong because β-lactams such as amoxicillin-clavulanate are second-line therapy, appropriate only when other recommended agents cannot be used, due to inferior efficacy and more adverse effects compared with other urinary tract infection antimicrobials (Talley & Langley, 2021, p. 639).

All previously discussed treatments apply to the geriatric population with the exception of fluoroquinolones, which are contraindicated or used as a last resort due to tendon and aortic rupture, in addition to contributing to mental status changes (Talley & Langley, 2021, p. 643).

Geriatric patients also present differently, and nursing home patients are more likely to have resistant pathogens compared with others of the same age (Talley & Langley, 2021, p. 643).

Choice a is wrong because cephalosporins such as ceftriaxone and cefepime are used for complicated urinary tract infections in this population and are not restricted in the way fluoroquinolones are (Talley & Langley, 2021, p. 640).

Choice b is wrong because aminoglycosides may be added initially for a complicated upper urinary tract infection, although they should not be used as monotherapy for pyelonephritis; they are not withheld as a class in the elderly (Talley & Langley, 2021, pp. 640–641).

Choice c is wrong because penicillins such as piperacillin/tazobactam and ampicillin are used in complicated urinary tract infections and are also preferred in pregnancy (Talley & Langley, 2021, pp. 640–641).

The KDIGO system is the current preferred three-stage system and is based on serum creatinine or baseline change, urine output volume, and glomerular filtration rate decreases in those younger than 18 years of age (Branham & Hilliard, 2021, p. 646).

KDIGO stage 1 is defined by a serum creatinine 1.5–1.9 times baseline, or an increase of at least 0.3 mg/dl, and a urine output less than 0.5 ml/kg/hr for 6–12 hr (Branham & Hilliard, 2021, p. 646).

Choice b is wrong because stage 2 requires a serum creatinine 2.0–2.9 times baseline and a urine output less than 0.5 ml/kg/hr for 12 hr (Branham & Hilliard, 2021, p. 646).

Choice c is wrong because stage 3 requires a serum creatinine 3.0 times baseline, a serum creatinine of at least 4.0 mg/dl, initiation of renal replacement therapy, or a urine output less than 0.3 ml/kg/hr for 24 hr or anuria for at least 12 hr (Branham & Hilliard, 2021, p. 646).

Choice d is wrong because the patient does meet the criteria for AKI; an acute increase in serum creatinine from baseline of at least 0.5 mg/dl has occurred, and this increase of 0.7 mg/dl exceeds the KDIGO threshold (Branham & Hilliard, 2021, pp. 646–647).

Prerenal AKI accounts for 60% of cases and is characterized by diminished renal perfusion from a decrease in blood supply to the kidneys, with no nephron damage present (Branham & Hilliard, 2021, p. 647).

Prerenal AKI results in increased tubular sodium and water reabsorption in an attempt to re-expand circulating blood volume, producing oliguria, a decreased urine sodium of less than 20 mEq/L, a high urine osmolality of greater than 500 mOsm/L, an increased urine-specific gravity of greater than 1.020, and an increased BUN-to-creatinine ratio of at least 20:1 (Branham & Hilliard, 2021, pp. 647–648).

Choice a is wrong because intrinsic AKI produces a urine sodium greater than 20 mEq/L, an isotonic urine osmolality of 350 mOsm or less, a BUN-to-creatinine ratio less than 20:1, and a fractional excretion of sodium greater than 1% (Branham & Hilliard, 2021, pp. 650–651).

Choice c is wrong because postrenal AKI is associated with obstruction of urinary flow, and the urine volume may fluctuate between anuria and polyuria with a variable fractional excretion of sodium and hydronephrosis on ultrasound (Branham & Hilliard, 2021, p. 652).

Choice d is wrong because chronic kidney disease is a progressive azotemia over weeks, months, or years with a glomerular filtration rate of 60 ml/min or less for longer than 3 months, which does not describe this acute presentation after volume loss (Branham & Hilliard, 2021, p. 661).

Acute tubular necrosis accounts for most hospital-associated cases of intrinsic AKI, around 85–90%, and is usually caused by prolonged periods of renal azotemia leading to tubular injury (Branham & Hilliard, 2021, p. 649).

The urine sediment in acute tubular necrosis often contains granular casts, described as muddy brown casts, along with renal tubular epithelial cells (Branham & Hilliard, 2021, pp. 649, 655).

Choice a is wrong because acute tubulointerstitial nephritis accounts for 10–15% of cases of intrinsic renal failure, and more than 70% of cases are related to drug-induced hypersensitivity, with urine sediment showing eosinophilia, renal tubular epithelial casts, and a fractional excretion of sodium greater than 1% (Branham & Hilliard, 2021, pp. 650–651).

Choice b is wrong because prerenal azotemia reflects diminished renal perfusion without nephron damage and produces a bland sediment with no casts or only occasional hyaline casts (Branham & Hilliard, 2021, pp. 647–648).

Choice d is wrong because acute glomerulonephritis produces red blood cell casts and proteinuria, and it is more commonly associated with immunologic disorders such as systemic lupus erythematosus (Branham & Hilliard, 2021, pp. 649, 651).

Contrast-induced nephropathy is defined as a rise in serum creatinine between 25% and 50% within 48 hr of intravenous contrast, and fluid administration is supported by high-level evidence (Branham & Hilliard, 2021, p. 649).

Isotonic intravenous fluid administration is beneficial to prevent contrast-induced AKI, and normal saline or sodium bicarbonate have proven beneficial over 0.45% normal saline; if normal saline is selected, 1 ml/kg/hr should be given 6–12 hr before the contrast and 1 ml/kg/hr for 6–12 hr after the procedure (Branham & Hilliard, 2021, pp. 649–650).

Choice a is wrong because intravenous or oral N-acetylcysteine 600 mg every 12 hr for 48–72 hr has been used to prevent contrast-induced injury, but it has not been shown to be superior to fluid alone, and results are inconsistent across studies and meta-analyses (Branham & Hilliard, 2021, p. 650).

Choice b is wrong because diuretics such as mannitol and furosemide have not shown a benefit and may be harmful (Branham & Hilliard, 2021, p. 650).

Choice c is wrong because discontinuation of angiotensin-converting enzyme inhibitors has not been found to prevent contrast-related injury; in diabetic patients, metformin or combinations containing the drug should instead be withheld for 48 hr prior to the dye load (Branham & Hilliard, 2021, p. 650).

Hyperkalemia treatment should be considered when the serum potassium is above 5.5 mEq/L or in the presence of potassium-related electrocardiogram changes of peaked T waves, loss of P waves, PR or QRS widening, or bradycardia (Branham & Hilliard, 2021, p. 658).

Interventions to antagonize the proarrhythmic effects of hyperkalemia include intravenous administration of calcium, such as 10 ml of a 10% solution of calcium gluconate, which is cardioprotective, temporarily reverses the neuromuscular effects of hyperkalemia, and is felt to have the fastest onset of action; it should be avoided if digoxin toxicity is suspected (Branham & Hilliard, 2021, p. 658).

Calcium gluconate 10% 1 g given intravenously over 1–2 min has an immediate onset, does not lower the serum potassium, and lasts for minutes only, so it is repeated in 3–5 min if needed to normalize the electrocardiogram (Culpepper, 2021, p. 1241).

Choice a is wrong because regular insulin 10 units with dextrose drives potassium into the intracellular space, lowering serum potassium without lowering total body potassium, and its effect appears within 15–30 min rather than immediately (Branham & Hilliard, 2021, p. 658; Culpepper, 2021, p. 1241).

Choice c is wrong because sodium polystyrene sulfonate (Kayexalate) is a gastrointestinal binding agent that lowers total body potassium gradually through the distal colon and rectum, and it has no role in the emergency treatment of electrocardiogram changes (Branham & Hilliard, 2021, pp. 658–659).

Choice d is wrong because intravenous sodium bicarbonate is felt to be most useful in lowering potassium when metabolic acidosis is present, and it is not considered first-line hyperkalemia treatment unless metabolic acidosis is present (Branham & Hilliard, 2021, p. 658).

Chronic kidney disease is defined as a glomerular filtration rate of 60 ml/min or less for longer than 3 months, with or without kidney damage, or kidney dysfunction with one of the following: albuminuria, urine sediment abnormalities, electrolyte abnormalities related to tubular disorders, abnormal histology, abnormal kidney structures on repeat imaging, or a history of renal transplant (Branham & Hilliard, 2021, p. 661).

Stage 3a is described as a mild to moderate decrease in glomerular filtration rate, corresponding to 45–59 ml/min/1.73 m² (Branham & Hilliard, 2021, p. 661).

Choice a is wrong because stage 1 is kidney damage, such as protein in the urine, with a normal glomerular filtration rate greater than 90 ml/min/1.73 m² (Branham & Hilliard, 2021, p. 661).

Choice b is wrong because stage 2 is kidney damage with a mild decrease in glomerular filtration rate of 60–89 ml/min/1.73 m² (Branham & Hilliard, 2021, p. 661).

Choice d is wrong because the stage that follows 3b corresponds to a glomerular filtration rate of 15–29 ml/min/1.73 m², which is well below this patient's value; note that Table 43.5 in the assigned reading labels that row "3" where the standard classification labels it stage 4, an error in the source text (Branham & Hilliard, 2021, p. 661).

Peritoneal dialysis is contraindicated in pregnancy, active inflammatory bowel disease, and placement of abdominal ostomies (Branham & Hilliard, 2021, p. 661).

Peritoneal dialysis is beneficial for long-term use and improves quality of life over conventional dialysis methods by promoting patient autonomy and greater independence with scheduling, with overall decreased cost for supplies compared with hemodialysis (Branham & Hilliard, 2021, pp. 660–661).

Choice b is wrong because diabetes mellitus is a common cause of chronic kidney disease through diabetic nephropathy and is not a contraindication to peritoneal dialysis (Branham & Hilliard, 2021, pp. 660–662).

Choice c is wrong because hypertension is common in most patients with chronic kidney disease and is not a contraindication to peritoneal dialysis (Branham & Hilliard, 2021, pp. 660, 662).

Choice d is wrong because heart failure, while a consideration for volume management, is not among the listed contraindications; the limitations of peritoneal dialysis are its lower creatinine clearance rates, which may require conversion to an alternate method in catabolic states such as major surgery, burns, or sepsis, and its high risk for catheter site and intra-abdominal infections (Branham & Hilliard, 2021, pp. 660–661).

The ability of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers to reduce proteinuria is up to 35–40% greater than that of the other antihypertensives, making them the antihypertensive agents of choice for all patients with chronic kidney disease who have an albumin excretion rate of 30 mg/day or more, unless contraindicated (Branham & Hilliard, 2021, p. 664).

Antihypertensive agents that maintain renal blood flow and reduce glomerular pressure and proteinuria are preferred, and the goal blood pressure for patients with chronic kidney disease is less than 140/80 mm Hg, or less than 125/75 mm Hg for those with proteinuria of 1–2 g (Branham & Hilliard, 2021, p. 664).

Choices a, b, and c are wrong because although these classes may be used to control blood pressure, none of them reduces proteinuria or glomerular pressure to the degree that angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers do (Branham & Hilliard, 2021, p. 664).

Anemia in chronic kidney disease is due to erythropoietin deficiency, and all correctable causes must be identified and treated first, with iron given orally or intravenously based on iron studies (Branham & Hilliard, 2021, pp. 663, 666).

For nondialysis patients, an erythropoiesis-stimulating agent should not be initiated when the hemoglobin is greater than 10 g/dl, and it should be held when the hemoglobin is greater than 11 g/dl (Branham & Hilliard, 2021, p. 667).

Choice a is wrong because targeting a higher hemoglobin with these agents is not recommended; black box warnings indicate an increased risk of stroke, severe hypertension, and loss of vascular access, all of which can lead to death (Branham & Hilliard, 2021, p. 666).

Choice c is wrong because iron therapy is guided by iron studies after correctable causes are identified, and it does not justify continuing the erythropoiesis-stimulating agent above the threshold at which it should be held (Branham & Hilliard, 2021, pp. 666–667).

Choice d is wrong because transfusion is not indicated at a hemoglobin of 11.6 g/dl; the recommendation at this level is to hold the erythropoiesis-stimulating agent (Branham & Hilliard, 2021, p. 667).

Before administering any drug to a patient in renal failure, the practitioner should consider whether the drug depends on the kidney for excretion, whether an excess blood level affects the kidney or causes nephrotoxicity, whether the effect of the drug alters electrolyte imbalance, and whether the patient is susceptible to the drug because of kidney disease (Branham & Hilliard, 2021, p. 668).

Drugs are also classified by their route of elimination: type A drugs are eliminated entirely by the kidney, type B drugs are eliminated entirely by extrarenal mechanisms, and type C drugs are eliminated by both renal and extrarenal mechanisms (Branham & Hilliard, 2021, p. 668).

Choice a is wrong because the route of administration is not one of the four considerations; the concern is whether the drug depends on the kidney for excretion (Branham & Hilliard, 2021, p. 668).

Choice b is wrong because therapeutic drug monitoring, while useful in practice, is not one of the four questions the source identifies for the patient in renal failure (Branham & Hilliard, 2021, p. 668).

Choice d is wrong because a prior adverse reaction is part of a general medication history, not one of the four considerations specific to renal failure (Branham & Hilliard, 2021, p. 668).

The rate of correction of serum sodium is critical, because overcorrection or a very rapid rise in serum sodium may inflict further central nervous system injury, as seen in the osmotic demyelination syndrome formerly known as pontine myelinolysis (Culpepper, 2021, p. 1232).

With seizures or coma and a serum sodium less than 120 mEq/L, water or total fluid intake is restricted to 1,000 ml/24 hr or less, and 3% hypertonic saline is then infused at a rate of 0.5–2 ml/kg/hr to increase the serum sodium by 1–2 mEq/L/hr until the sodium rises by a maximum of 12 mEq/L in the first 24 hr; the maximum correction rate is 8–12 mEq/L/24 hr, or 20 mEq/L/48 hr (Culpepper, 2021, p. 1233).

Choice a is wrong because a 4–6 mEq/L rise describes the initial bolus target, in which 100 ml of 3% saline is given over 10 min and repeated up to two times as needed to achieve a 4–6 mEq/L rise or until symptoms improve, not the maximum rate over 24 hr (Culpepper, 2021, p. 1233).

Choice b is wrong because 20 mEq/L is the maximum correction over 48 hr, not over 24 hr (Culpepper, 2021, p. 1233).

Choice c is wrong because rapid normalization of the serum sodium risks osmotic demyelination syndrome, and the serum sodium should be corrected gradually (Culpepper, 2021, pp. 1232–1233).

The electrocardiogram in hypokalemia shows T wave flattening and the appearance of a U wave (Culpepper, 2021, p. 1238).

Serum magnesium is decreased in up to 40% of hypokalemic patients, and it requires correction to effectively replete body potassium (Culpepper, 2021, p. 1238).

Chronic alcohol use carries a 30% incidence of hypomagnesemia, and alcohol withdrawal carries an 80–85% incidence, so this patient is at high risk for the magnesium deficiency that prevents effective potassium repletion (Culpepper, 2021, p. 1246).

Choice b is wrong because peaked T waves, a widened QRS complex, disappearance of the P wave, and fusion of the QRS and T waves to form a sine wave are the electrocardiographic findings of hyperkalemia, whereas T wave flattening with a U wave indicates hypokalemia (Culpepper, 2021, pp. 1238, 1240).

Choice c is wrong because magnesium deficiency must be corrected for potassium repletion to be effective, and a serum magnesium of 1.2 mg/dl is below the normal range of 1.5–2.5 mg/dl (Culpepper, 2021, pp. 1238, 1246).

Choice d is wrong because the maximum infusion rate is 20 mEq/hr for a peripheral infusion and 40 mEq/hr for a central infusion, with a maximum concentration of 40 mEq/L for peripheral vein infusion and 60 mEq/L for central vein infusion, and continuous electrocardiogram monitoring is required (Culpepper, 2021, p. 1238).

Calcium gluconate 10% 1 g given intravenously over 1–2 min antagonizes the hyperkalemic effect with an immediate onset, does not lower serum potassium, and its effect lasts for minutes only, so it is repeated in 3–5 min if needed to normalize the electrocardiogram (Culpepper, 2021, p. 1241).

Calcium chloride may also be given through a central line, but the dose needs to be adjusted to prevent calcium toxicity because it contains about three times the amount of calcium per 10 ml dose compared with calcium gluconate, and serum calcium should be monitored with each recheck of serum potassium (Culpepper, 2021, p. 1241).

Choice a is wrong because calcium neither lowers serum potassium nor total body potassium; insulin with dextrose, albuterol, and sodium bicarbonate shift potassium into cells without lowering total body potassium, and diuretics, gastrointestinal binders, or dialysis are required to remove it (Culpepper, 2021, pp. 1241–1242).

Choice c is wrong because the effect of calcium lasts only minutes, so it is repeated in 3–5 min if needed, and other measures are required to lower the serum potassium (Culpepper, 2021, p. 1241).

Choice d is wrong because an absent P wave, QRS widening, or sine waves are the specific indications for intravenous calcium (Culpepper, 2021, p. 1241).

A portion of total calcium binds to serum albumin, so serum calcium is corrected upward by 0.8 mg/dl for each 1 g/dl decrease in serum albumin, and the normal total calcium range is 8.6–10.2 mg/dl (Culpepper, 2021, p. 1242).

Because this patient's albumin is 2.0 g/dl, a decrease of 2.0 g/dl from the reference value of 4.0 g/dl, the correction adds 1.6 mg/dl to the measured value, giving a corrected serum calcium of 9.0 mg/dl.

Choice a is wrong because the albumin-bound fraction of calcium is not physiologically active, so the total serum calcium must be corrected for a low serum albumin; the physiologically active fraction is the ionized calcium, with a normal range of 4.6–5.3 mg/dl, or 1.12–1.30 mmol/L (Culpepper, 2021, p. 1242).

Choice b is wrong because the correction is applied upward rather than downward, and symptomatic hypocalcemia presents with mental changes, tetany, seizures, weakness, Chvostek's sign, and Trousseau's sign, none of which this patient has (Culpepper, 2021, pp. 1242–1243).

Choice d is wrong because the corrected value of 9.0 mg/dl is within the normal range; hypercalcemia is defined by a total serum calcium corrected for serum albumin of greater than 10.2 mg/dl, or an ionized calcium greater than 5.3 mg/dl (Culpepper, 2021, pp. 1242, 1244).

The anion gap is calculated as the serum sodium minus the sum of the chloride and bicarbonate, with a normal anion gap of 8–10 mEq/L (Culpepper, 2021, p. 1251).

For this patient, 138 − (96 + 14) = 28 mEq/L, which indicates a high anion gap metabolic acidosis; a high anion gap metabolic acidosis has an anion gap greater than 15 mEq/L and indicates the addition to serum of a nonchloride acid anion such as lactate (Culpepper, 2021, pp. 1251–1252).

Endogenous causes of a high anion gap metabolic acidosis include lactic acidosis from hypoxia, sepsis, or circulatory shock; diabetic ketoacidosis from a lack of insulin; alcoholic ketoacidosis from a drinking binge ending in nausea and vomiting with poor nutrition; and stages 4–5 chronic kidney disease with a glomerular filtration rate less than 15–20 ml/min or acute kidney injury (Culpepper, 2021, p. 1252).

Choice a is wrong because a normal anion gap metabolic acidosis has an anion gap less than 12 mEq/L and indicates primary bicarbonate loss or hydrogen plus chloride gain, as occurs with diarrhea, pancreatic drainage, or renal tubular acidosis (Culpepper, 2021, pp. 1251–1252).

Choice b is wrong because the pH of 7.28 is below 7.35, indicating acidemia rather than alkalemia, and metabolic alkalosis is identified by a bicarbonate level exceeding 28 mEq/L (Culpepper, 2021, pp. 1251, 1253).

Choice c is wrong because the pCO2 of 30 mm Hg is below the normal range of 35–45 mm Hg and represents respiratory compensation for the metabolic acidosis; a primary respiratory acidosis would be identified by a pCO2 greater than 45 mm Hg (Culpepper, 2021, pp. 1251, 1255).

5% dextrose in water is approximately isotonic to plasma, distributes to intracellular and extracellular body water spaces, and is used for repletion or maintenance of body water, making it equivalent to giving pure water once the dextrose has metabolized; less than 10% of the infused volume remains in the vascular space at full distribution (Culpepper, 2021, p. 1260).

For mild volume depletion with hypernatremia, intravenous 5% dextrose in water is the appropriate choice, and hyperglycemia and glucosuria should be avoided to prevent further renal water loss (Culpepper, 2021, p. 1236).

Choice b is wrong because 0.9% normal saline is used for volume resuscitation in shock, sepsis, hemorrhage, or burn patients and for fluid challenges in hypotensive or oliguric patients; approximately one third of the infused volume remains in the vascular space to support circulatory function, so it expands the extracellular fluid volume rather than depleting the free water deficit (Culpepper, 2021, p. 1260).

Choice c is wrong because lactated Ringer's solution distributes to the extracellular fluid compartment and is used mainly as a repletion or resuscitation fluid in the face of actual or ongoing blood loss, such as in trauma or surgical patients (Culpepper, 2021, p. 1260).

Choice d is wrong because colloid solutions such as 25% human albumin are expensive, are used for selective vascular volume expansion and hemodynamic support, and offer little advantage for use in most patients over crystalloids (Culpepper, 2021, p. 1261).