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Renal Disease and HIV

for Health Care Providers

Renal Disease

Note: Some medications mentioned in this chapter may not be available on the VHA National Formulary. Consult VA pharmacists for alternatives.

Key Points

  • At the time of HIV diagnosis, all patients should be screened for renal dysfunction with a urinalysis (UA) and a calculated estimate of renal function.
  • Elevated risk of developing kidney disease: African American race, hypertension, diabetes, family history, CD4 count <200 cells/µL, unsuppressed viral load, hepatitis C virus (HCV) infection. Persons meeting any of these criteria should be screened annually.
  • Chronic kidney disease (CKD) increases the risk of developing cardiovascular disease.
  • Patients with CKD should be referred to a nephrologist for evaluation and possible renal biopsy.
  • HIV-infected persons with CKD are less likely to receive ART, even when ART is indicated.
  • HIV-associated nephropathy (HIVAN) is an indication to start ART.
  • Acute renal failure (ARF) usually is attributable to prerenal causes or medication toxicity leading to acute tubular necrosis (ATN) (see Table 3).
  • Dosage of most NRTIs should be adjusted for impaired renal function (see Table 2).

Background

  • There is a high prevalence (30%) of abnormal renal function among patients with HIV disease.
  • CKD is increasingly a cause of morbidity among people with HIV infection.
  • Risk factors for CKD include African American race, hypertension, diabetes, family history of CKD, CD4 count <200 cells/µL, unsuppressed viral load, and HCV infection.
  • Risk factors for HIVAN include African American race, low CD4 cell count, and family history of CKD. Prevalence of HIVAN is 3.5% among HIV-infected African American patients.
  • African Americans are disproportionately affected by kidney disease.
  • HIV-infected persons with CKD are less likely to receive ART, even when ART is indicated.
  • ART should be given to patients with renal disease, if indicated, though most NRTIs must be dosed according to renal function and some ARVs should be avoided (see Table 2 and Table 3).

Veterans with HIV*

Renal failure, acute: 7%

Renal failure, chronic: 6%

*Veterans in the VA HIV Clinical Case Registry in care in 2007 with an ICD-9 code corresponding to these conditions

Screening

  • All HIV-infected patients should be screened for kidney disease at the time of HIV diagnosis or entry into care.
  • Patients with additional risk factors or exposure to nephrotoxic medications (including TDF) should be screened every 3-6 months. Those with stable renal function on ART without nephrotoxic medications should be screened every 3-12 months.
  • Individuals without risk factors may be rescreened based on clinical signs and symptoms.
  • Screening tests: calculated estimate of renal function, UA, and quantitative spot measurement of proteinuria.
  • If screening shows creatinine clearance (CrCl) or estimated GFR (eGFR) <60 mL/min/1.73 m2, or proteinuria ≥1+ on urine dipstick analysis, calculate spot urine albumin-to-Cr ratio or spot urinary protein-to-Cr (described below), obtain renal ultrasound to look for anatomic abnormalities (including size), and consider referral to nephrologist for management and possible biopsy.

1. Estimate renal function:

  • The first evidence of renal dysfunction may be an elevated serum Cr (SCr) level. Increases in SCr from baseline should prompt an evaluation.
  • In many patients, SCr may not be an accurate measure of renal function:
    • May be deceptively low in the elderly and persons with low muscle mass
    • May be deceptively high in African Americans and persons with high muscle mass
  • A calculated estimate of renal function is a better measure because it corrects for these variations.
  • The simplified Modification of Diet in Renal Disease (MDRD) Study equation for eGFR is thought to yield a more accurate estimate of renal function than the Cockcroft-Gault equation, which measures CrCl, a proxy for GFR.
  • CrCl typically is used to determine medication dosage adjustments in patients with renal insufficiency.

Simplified MDRD Equation for Estimating Renal Function

GFR (mL/min/1.73 m2) = 186 x [serum creatinine (mg/dL)]-1.154 x
[age (years)]-0.203 x [0.742 if female] x [1.212 if African American]

Normal GFR:≥90 mL/min/1.73 m2

CKD: GFR <60 mL/min/1.73 m2

2. Perform urinalysis (dipstick or formal); look especially for proteinuria and hematuria (see Urology, for evaluation of isolated hematuria).

Dipstick Interpretation in Setting of Abnormal eGFR

ProteinBloodConsider
NegativeNegative
PositiveNegative
  • False positive
  • Benign or orthostatic proteinuria, hypertension, nephrosclerosis, diabetes, tubulointerstitial diseases, polycystic kidney disease (PCKD), nephrotic syndrome, glomerulonephritis (GN)
PositivePositiveUTI, pyelonephritis, rapidly progressive GN, other GN, HIV-associated vasculitis, pulmonary-kidney syndrome, hemolytic-uremic syndrome, thrombotic thrombocytopenic purpura, malignant hypertension, nephrotic syndrome, nephrolithiasis with obstruction, atypical diabetes, PCKD

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Quantitate proteinuria:

  • Evaluate patients with ≥1+ protein on dipstick or GFR <60 mL/min/1.73 m2.
  • Dipstick UA is insensitive for microalbuminuria (albuminuria below level detected by conventional dipsticks).
  • Microalbuminuria may be the first indication of renal dysfunction; if detected, treatment to slow progression of renal disease should be started (see below).
  • Timed (ie, 24-hour) collections have largely been replaced by:
    1. The random urinary albumin-to-Cr ratio: AlbuminUrine [mg/dL]/ CrUrine [mg/dL]
      Highly sensitive for microalbuminuria; normal is <0.03. Should be used at initial screening and for follow-up, if microalbuminuria is diagnosed.
    2. The random urinary protein-to-Cr ratio: ProteinUrine [mg/dL] / CrUrine [mg/dL]
      Highly sensitive for proteinuria, but not for microalbuminuria; normal is <0.15.
      Used to estimate 24-hour urine protein excretion (the ratio corresponds to grams of urinary protein excreted per 24 hours; eg, ratio of 0.15 corresponds to 0.15 g [150 mg] of proteinuria per 24 hours). Can be used to grade degree of proteinuria (see box below); can be monitored over time.

      Note: these estimates may be inaccurate in muscular or cachectic patients.
Degree of Proteinuria Based on Spot Urinary Protein-to-Cr Ratio
Normal:<150 mg/24 hours
Trace proteinuria:150-500 mg/24 hours
Mild proteinuria:500 mg to 1 g/24 hours
Moderate proteinuria:1-3 g/24 hours
Nephrotic range proteinuria:>3 g/24 hours
  • Patients with significant proteinuria should be referred for further evaluation

Types of Proteinuria

Overflow proteinuria: Trace or negative dipstick protein but disproportionately larger amount on 24-hour test. Suggests light-chain disease, paraproteinemia, lymphoproliferative process, or hemolysis (if dipstick is also positive for blood).

Tubular protein: 500-2,000 mg/24 hours

Differentiate from glomerular causes by UPEP +/- IEP.

  • UPEP: albumin > globulin suggests glomerular proteinuria; globulin > albumin suggests light chains or paraproteinemia

Common causes include analgesic nephropathy, focal glomerular sclerosis (recurrent UTI, reflux), collagen vascular diseases (Sjögren syndrome, lupus), hepatitis, HIVAN (see below), PCKD, heavy metal toxicity, interstitial nephritis (drugs or infectious), granulomatous diseases.

Glomerular protein, suggested by moderate to heavy proteinuria:

Suggests a more serious disorder. Rule out HIVAN, diabetes progression, hepatitis, vasculitis, malignancy, GN. Significant glomerular damage with proteinuria of >3 g: refer to nephrologist.

Massive proteinuria:>6 g/24 hours

Focus evaluation on HIVAN, hepatitis-associated nephropathy, severe focal glomerulosclerosis. Refer to nephrologist.

Chronic Kidney Disease

Evaluation

  • CKD is characterized by the presence for ≥3 months of either of the following:
    • Structural or functional kidney abnormalities, with or without decreased GFR, as diagnosed by abnormal pathology or abnormal markers. Markers can include blood or urine abnormalities (urinary protein, red blood cells, white blood cells, casts, fat) or abnormalities on imaging studies.
    • GFR <60 mL/min/1.73 m2, with or without other evidence of kidney damage (see simplified MDRD equation, above).
  • Proteinuria and eGFR <60 mL/min/1.73 m2 are associated with increased cardiovascular disease and increased all-cause mortality.
  • Treatment of early-stage CKD in HIV-noninfected persons slows progression of kidney disease.
  • CKD has 5 stages, based on estimated renal function (see Table 1).
Table 1. National Kidney Foundation Stages of Chronic Kidney Disease (based on eGFR)
StageDefinitioneGFR (mL/min/1.73 m2)Recommendations
* Dialysis usually is initiated when eGFR falls below 10 mL/min/1.73 m2.
1Kidney damage with normal eGFR≥90Treat comorbid conditions; slow progression of CKD; reduce cardiovascular risk factors
2Kidney damage with mildly decreased eGFR60-89Estimate progression of CKD
3Kidney damage with moderately decreased eGFR30-59Evaluate and treat complications of CKD
4Kidney damage with severely decreased eGFR15-29Prepare for renal replacement therapy (RRT; dialysis)
5Kidney failure*<15*RRT, if uremia present*

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Evaluation of CKD

Risk factors
  • Diabetes
  • Hypertension
  • Toxic insults (including medications)
  • Autoimmune disease
  • HCV infection
  • Inherited kidney disease (eg, pckD)
  • HIVAN (see below)
  • Chronic urinary tract obstruction
  • Paraproteinemias
  • ARF
History
  • Chronic medical problems: diabetes, hypertension, prior kidney disease, collagen vascular disease, hepatitis, kidney stones, prostate disease
  • Symptoms associated with kidney disease, such as: decreased attentiveness, nausea, vomiting, anorexia, weight change, dyspnea, orthopnea, leg swelling, fatigue, muscle cramps, restless legs, peripheral neuropathy, pruritus, urinary urgency or frequency, nocturia, dysuria, oliguria
  • Medications and over-the-counter products: NSAIDs, ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), diuretics, analgesics, antibiotics, antiviral agents, lithium
Physical examination
  • Height, weight
  • Vital signs including orthostatic blood pressure
  • Volume assessment (rales, jugular venous distention, peripheral edema)
  • Cardiac exam (S3, S4, heave, murmur, rub)
  • Vascular exam (pulses, bruits)
  • Abdominal findings (mass, bruit, palpable bladder, flank tenderness)
  • Digital rectal exam (prostate) in men
  • Neurological exam, including mental status
  • Integument (rash, stigmata of embolic disease or ischemia)
  • Joints (arthritis)
Diagnostic testing
  • eGFR, urinalysis, spot urine albumin-to-Cr ratio or protein-to-Cr ratio, as above
  • Renal ultrasound
  • Basic workup for non-HIV-related causes:
    • Hepatitis B and C serologies
    • Cryoglobulins
    • SPEP/UPEP
    • Fasting blood glucose
    • Complement levels
    • Antinuclear antibodies and antineutrophil cytoplasmic antibodies
      (Note: significant false-positive rates in HIV-infected persons)
When to Refer
  • Refer promptly to nephrologist for possible biopsy and for directing appropriate therapy, particularly if HIVAN is suspected
  • HIVAN can progress rapidly from proteinuria to end-stage renal disease (ESRD), and requires biopsy for unequivocal diagnosis (see HIV-Associated Nephropathy, below)
  • Biopsy also can distinguish HIVAN from other HIV-related causes of CKD, such as immune complex disease and thrombotic angiopathy, as well as non-HIV-related causes of CKD

Management

  • Goals:
    • Slow progression of CKD
    • Address metabolic and hematologic abnormalities
  • Determine whether patient has signs/symptoms of ARF (see below).
  • Maintain blood pressure at ≤130/80 mmHg.
  • Initiate ACEIs or ARBs for patients with hypertension or proteinuria (see Hypertension for dosing information).
    • Closely monitor patients on ACEIs and ARBs for hyperkalemia.
  • ART:
    • Initiate or maximize efficacy of ART if diagnosis of HIVAN is established (see below).
    • Avoid ARVs with significant renal toxicity (see below).
    • Adjust dosing of ARVs (see below) and other drugs (eg,TMP-SMX, H2 receptor antagonists) for renal function, as needed.
  • Avoid NSAIDs and other nephrotoxic medications.
  • Screen for and/or maximize treatment for diabetes and dyslipidemia (see Diabetes and Dyslipidemia.
  • Screen for and treat hematologic abnormalities (eg, anemia).
  • Advise on protein- and salt-restricted diet; refer to renal dietitian to avoid malnutrition.
  • Refer for substance abuse counseling, when appropriate, to decrease risk of nephropathy associated with use of heroin or other illicit substances.
  • Monitor renal function; consult Nephrology regarding other care.
  • Refer patients with moderate to advanced CKD for RRT (ie, dialysis) or kidney transplantation.
    • Early referral and counseling for RRT improve outcomes.
    • HIV-infected and HIV-uninfected ESRD patients have similar outcomes.
    • Refer before Cr rises to 4 or eGFR falls below 25 mL/min.
    • Refer at least 6 months before anticipated need for RRT (plot inverse of Cr vs time to define likely rate of progression).
    • Referral for transplantation may be made to the VA National Transplant Program.

HIV-Associated Nephropathy

Evaluation

  • Occurs almost exclusively in persons of African descent. Other risk factors include low CD4 cell count, high HIV RNA.
  • Much less common since more widespread use of combination ART.
  • Among African American men, between 1995 and 1999, incidence of HIVAN decreased whereas prevalence and survival increased, which is consistent with a beneficial effect of ART on preventing and treating HIVAN.
  • Most often presents as nephrotic syndrome, with proteinuria and decreased GFR. May progress rapidly to ESRD, often over the course of several weeks to months (especially in patients not on ART).
  • Peripheral edema may be present.
  • Imaging typically shows large echogenic kidneys.
  • Biopsy shows collapsing focal segmental glomerulosclerosis with tubular and interstitial damage.

Management

  • Goal:
    • Slow progression of HIVAN
  • All patients with HIVAN should be started on ART regardless of CD4 count.
  • Refer immediately to a nephrologist for evaluation (including biopsy) and possible treatment.
  • For patients with hypertension or proteinuria, treat with ACEIs or possibly ARBs to reduce blood pressure to <125/75 mmHg, and to eliminate or decrease proteinuria as much as possible.
  • Closely monitor patients on ACEIs and ARBs for hyperkalemia.
  • Consider adding corticosteroids if renal function fails to improve on ART (consult with nephrologist). Recommended prednisone dosage is 1 mg/kg/day, to a maximum dosage of 80 mg/day. Treatment duration is 2 months, with a 2-4 month taper.
  • Refer patients with progressive disease for dialysis or transplantation.

Acute Renal Failure

Evaluation

  • Definition of ARF:
    • Decrease in eGFR of ≥25% over the course of days to weeks.
  • In a prospective cohort of HIV-infected outpatients, incidence of ARF was 5.9 cases per 100 person-years. The most common causes of ARF were a prerenal state and acute tubular necrosis (ATN).

    Risk factors
    • Male sex
    • HCV coinfection
    • HIV viral load of >10,000 copies/mL
    • CD4 count of <200 cells/µL
    • Presence of an opportunistic infection
    • History of an AIDS diagnosis
    • Current or prior ART
  • May be asymptomatic, or may present with volume overload (dyspnea, orthopnea), hypertension, metabolic abnormalities, decreased urine output, anorexia, nausea, vomiting, or encephalopathy.

Possible Causes of ARF

Prerenal Causes

  • Hypovolemia: hemorrhage, dehydration attributable to diarrhea, vomiting, or inadequate fluid intake
  • Hypoperfusion: ischemia (septic shock, heart failure, cardiogenic shock); reduced oncotic pressure (hypoalbuminemia, anemia)

Intrinsic Renal Causes

  • Glomerulonephritis (any type)
  • ATN resulting from prolonged prerenal injury
  • ATN resulting from toxins, including nephrotoxic medications: IV radiographic contrast dye, pentamidine, amphotericin B, foscarnet, cidofovir, high-dose acyclovir, aminoglycosides, TDF
  • ATN resulting from rhabdomyolysis (crush injury, statins [including in association with PIs], fibrate derivatives, cocaine)
  • Acute interstitial nephritis (AIN) resulting from medications: TMP-SMX and other sulfa-containing compounds, beta-lactam antibiotics, rifampin, IDV, NSAIDs, salicylates, many other medications
  • AIN resulting from infection: streptococcus, cytomegalovirus (rare)

Postrenal Causes

  • External obstruction: retroperitoneal masses; ureteral compression, urethral compression or blockage (eg, severe benign prostatic hypertrophy)
  • Internal obstruction: crystal deposition, nephrolithiasis, clot

Management

  • Assess volume status and metabolic abnormalities.
  • Provide supportive care (dialysis if necessary) and treat the underlying processes causing ARF.
  • Dialysis is indicated for uremic pericarditis, encephalopathy, volume overload with pulmonary edema, hyperkalemia, or metabolic acidosis.

Selecting ARVs for Patients with Kidney Disease

  • ART generally should not be avoided because of kidney disease.
  • ART is indicated in patients with HIVAN.
  • Accumulating evidence suggests ART decreases the risk of kidney disease in HIV-infected patients.
  • NRTIs, except for ABC, are excreted renally; dosage should be based on steady-state CrCl or eGFR (see Table 2).
  • TDF has been associated with rare cases of ARF and Fanconi syndrome.
  • TDF also has been associated with slow decreases in eGFR, typically in patients with preexisting renal insufficiency (see Table 3).
  • Agents from other classes (NNRTI, PI, fusion inhibitor, integrase inhibitor, chemokine coreceptor antagonist) do not undergo significant renal excretion and do not require dosage adjustment in patients with renal insufficiency.
  • For patients undergoing hemodialysis:
    • Serum levels of the ATV and LPV, for unclear reasons, are substantially decreased in patients on hemodialysis.
      • Unboosted ATV should not be given, and neither ATV nor ATV/r should be given to HIV treatment-experienced patients.
      • LPV/r should not be given QD, and levels may be low in those with resistance to LPV.
    • Other PIs have not been well studied in hemodialysis.
    • NVP: Give an additional dose (200 mg) after each dialysis session.
  • IDV and (rarely) ATV have been associated with nephrolithiasis (see Table 3).
  • Note that other medications commonly given to HIV-infected patients may also cause renal dysfunction (see Table 3).
Table 2. NRTI Dosing for Patients with Decreased Renal Function (based on CrCl)
DrugStandard DosageAdjusted Dosage/Notes
Adapted from McNicholl IR, Rodriguez RA. Dosing of Antiretroviral Drugs in Adults with Renal Insufficiency and HemodialysisLink will take you outside the VA website. VA is not responsible for the content of the linked site.. San Francisco: University of California San Francisco, Center for HIV Information; 2010. Accessed April 1, 2011.
ABC300 mg PO BIDDosage adjustment for renal insufficiency does not appear necessary
ddI250-400 mg PO QD, depending on weightCrCl (mL/min)Weight ≥60 kgWeight <60 kg
≥60400 mg QD250 mg QD
30-59200 mg QD125 mg QD
10-29125 mg QD125 mg QD
<10125 mg QDformulation not suitable
Hemodialysis125 mg QDformulation not suitable
FTC200 mg PO QDCrCl (mL/min)
≥50200 mg QD
30-49200 mg Q48H
15-29200 mg Q72H
<15200 mg Q96H
Hemodialysis200 mg Q96H, give after dialysis
3TC150 mg PO BID or 300 mg PO QDCrCl (mL/min)
≥50150 mg BID or 300 mg QD
30-49150 mg QD
15-29150 mg first dose, then 100 mg QD
5-14150 mg first dose, then 50 mg QD
<550 mg first dose, then 25 mg QD
d4T20 mg to 40 mg PO BID, depending on weightCrCl (mL/min)Weight ≥60 kgWeight <60 kg
>5040 mg BID30 mg BID
26-5020 mg BID15 mg BID
10-2520 mg QD15 mg QD
Hemodialysis20 mg QD15 mg QD
TDF300 mg PO QDExperience in patients with CrCl <60 mL/min is limited. Preliminary data suggest:
CrCl (mL/min)
≥50300 mg QD
30-49300 mg Q48H
10-29300 mg twice weekly
Hemodialysis300 mg weekly
ZDV300 mg PO BIDCrCl (mL/min)
<15100 mg Q6-8H
Hemodialysis100 mg TID

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ARV and Other Medications Associated with Renal Dysfunction

A number of medications commonly prescribed for treatment of HIV infection or opportunistic illnesses may cause acute or chronic renal disease (see Table 3). Some of these should be avoided in patients with renal insufficiency.

Table 3. Renal Adverse Effects of Medications Commonly Taken by HIV-Infected Persons
DrugDisorder/ PathologyFindingsComments/ Suggestions
TDFTDF-associated renal insufficiency↑ Cr, usually small; slight (4% vs other NRTIs) decrease in eGFR over time
  • Of unclear clinical significance, but warrants monitoring of renal function.
  • May be associated with duration of HIV infection, concomitant RTV-boosted PIs (which boost TDF levels), preexisting renal dysfunction, or diabetes.
  • Check serum and urine electrolytes, eGFR, and UA before starting therapy; check serum electrolytes and eGFR every 3-6 months on TDF; check UA every 6 months. Consider more frequent monitoring in patients with eGFR ≤90 mL/min/1.73 m2, renally secreted drugs, RTV-boosted PIs, diabetes, or hypertension.
  • Adjust TDF dosage based on steady-state CrCl.
  • Rare, usually resolves with discontinuation of TDF, but can lead to permanent damage, ESRD.
  • May be more likely in patients with preexisting renal disease.
  • Check serum and urine electrolytes, eGFR, UA before starting therapy and every 6 months on therapy, especially in patients with eGFR ≤90 mL/min/1.73 m2, renally secreted drugs, RTV-boosted PIs (which boost TDF levels), diabetes, or hypertension.
Proximal tubular injury (ATN)Fanconi syndrome (metabolic acidosis, ↑ Cr, ↓ serum K+ and phosphate, ↑ urine bicarbonate, phosphate, and glucose)
ATVNephrolithiasisSymptoms of renal colic, dysuria, urgency; mild ↑ Cr; ATV-containing stones
  • Case reports.
  • Treat with hydration; if symptoms do not resolve, or if symptoms recur, may need to discontinue drug.
IDVAIN↑ Cr, pyuria
  • Usually resolves with drug discontinuation; may require steroids.
CrystalluriaAsymptomatic, or symptoms of renal colic, dysuria, urgency; crystals on UA; mild ↑ Cr
  • Treat with hydration.
  • If manifestations do not resolve, may need to discontinue drug.
  • Not necessary to discontinue for asymptomatic crystalluria.
NephrolithiasisRenal colic, dysuria, urgency; mild ↑ Cr; crystals on UA; stones or filling defects on radiography
  • Risk reduced by drinking 1.5-2 liters of liquids per day.
  • Treat with hydration; if symptoms do not resolve, or if symptoms recur, may need to discontinue drug.
AcyclovirCrystalluriaMay precipitate ARF
  • Treat with hydration; avoid rapid intravenous bolus; adjust dosage for renal function.
Amphotericin BIncreased tubular permeability and/or renal vasoconstriction↑ Cr, ↓ serum K+ and Mg++, ↓ urine bicarbonate; distal renal tubular acidosis; non-anion-gap metabolic acidosis
  • More severe renal failure likely with concurrent nephrotoxins (aminoglycosides, foscarnet), diuretic use, hypovolemia, chronic renal failure.
  • Hydration with normal saline is somewhat protective.
  • Switch to lipid formulation of amphotericin B for rise in Cr of >2.5 mg/dL while on conventional amphotericin B; continue to monitor electrolytes.
CidofovirProximal tubular injury(See TDF, above)
  • Incidence reduced with hydration (normal saline) and probenecid, which blocks absorption of drug by tubular epithelial cells.
  • Check Cr and urine protein within 48 hours before each dose and reduce dosage for decreased CrCl or eGFR.
  • Discontinue drug for either Cr ≥0.5 mg/dL above baseline or proteinuria ≥3+ on dipstick analysis.
FoscarnetATN
Crystal deposition
↑ Cr, ↓ serum Ca++, Mg++, phosphorus; sometimes↑ serum Ca++ and phosphorus
  • Cr generally increases after 1-2 weeks of foscarnet therapy.
  • Renal toxicity is reduced with infusion of 0.5-1 liter of normal saline with or before foscarnet.
  • Toxicity is more likely with concomitant nephrotoxins.
Pentamidine (IV, rarely aerosolized)Tubular toxicity (ATN)↑ Cr, ↑ serum K+; ↓ serum Mg++ and Ca++
  • Discontinuation of pentamidine reverses toxicity, although that process can take several weeks.
TMP-SMXHyperkalemia caused by blockage of Na+ channel in collecting tubule↑ Serum K+
  • Usually seen with high-dose therapy (eg, PCP treatment), but sometimes seen with lower dosages.
  • Hyperkalemia more common with preexisting renal insufficiency.
Impaired tubular secretion of Cr↑ Cr
  • Hyperkalemia often appears after 1 week of therapy.
  • Consider monitoring serum K+, especially with high-dose therapy.

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References