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Slideshare uses cookies to improve functionality and performance, and to provide you with relevant advertising. Several lines of evidence point to kidney disease as an important complication of human immunodeficiency virus (HIV) infection. However, clinical research in this emerging area has not yet matured to the point at which it can provide clear evidence on how best to treat these patients.
We recommend that all patients at time of HIV diagnosis be assessed for existing kidney disease with a screening urine analysis for proteinuria and a calculated estimate of renal function (creatinine clearance or glomerular filtration rate [GFR]) (C-III); a renal function estimate also allows the caregiver to properly prescribe those antiretrovirals and other commonly used medications that require renal adjustment.
Therapy for HIV-associated renal diseases should be individualized to the patient's clinical circumstances and to the underlying renal histology findings. Patients with HIV-associated nephropathy (HIVAN) should be treated with HAART at diagnosis (B-II).
Prednisone should also be considered in treating adult patients with refractory HIVAN (B-II), although steroids are not recommended for children with HIVAN (D-II). Preliminary data suggest that renal transplantation may be a viable treatment option for patients with ESRD and should be considered if provided in a supervised clinical trial or at centers with adequate experience in this area (C-III). Dialysis and the placement of arteriovenous fistulae should not be withheld for patients solely because of HIV infection (A-II). Among those patients at higher risk (see "Renal Effects of Commonly Used Medications in HIV Care" below in this article), biannual monitoring for renal function and urinary abnormalities is warranted for those receiving indinavir (B-II) or tenofovir (B-III). We first provide general reviews regarding the evaluation of renal disease and the epidemiology of CKD in the HIV-infected population; these are followed by specific recommendations for the management of cases in this population. Incidence and prevalence rates of HIV-infected patients with ESRD reported by various studies utilizing the USRDS database have demonstrated similar results [23, 24].
In addition to African American race [28-35], decreased CD4+ cell count [31, 36] and a family history of renal disease [37] are risk factors for the development of HIVAN. Recent data from the USRDS has demonstrated that the mortality rates for patients with AIDS-related nephropathy have improved, compared with mortality rates in pre-HAART era reports, and are now approaching the mortality rates in the general ESRD population.
The progression of HIVAN to ESRD can be quite rapid, and thus HIV-infected patients with CKD who have chosen hemodialysis should be referred early to a nephrologist and to a surgeon for placement of a native arteriovenous fistula. The incidence and spectrum of peritonitis has been reported in several small series of HIV-infected patients receiving peritoneal dialysis.
Preliminary short-term data in case reports and small cohorts of liver, kidney, and heart transplant recipients suggest that patient survival rates may be similar to those in HIV-uninfected transplant recipients, implying that immunosuppression may not be uniquely dangerous in the context of HIV infection [87, 88]. The optimal intensity of therapy, the potential effects of ARBs, and the specific benefits of ACE inhibitors on HIV-related kidney diseases other than HIVAN are unknown. The need to adjust the dosing of antiretrovirals in the patient with CKD is underappreciated by HIV caregivers [20].
On the other hand, the nonnucleoside reverse-transcriptase inhibitors (NNRTIs), protease inhibitors (PIs), and fusion inhibitors are, in general, much more tightly bound to plasma proteins and are primarily metabolized by the liver. Many of the antimicrobials commonly used to prevent and treat opportunistic infections such as Pneumocystis jiroveci pneumonia, Toxoplasma encephalitis, and Mycobacterium avium intracellulare infections require dose reduction in the HIV-infected patient with CKD because of their renal elimination. Most of the cases described in the literature occurred in subjects who were receiving prolonged courses of tenofovir plus ritonavir-containing combination therapy (including lopinavir, saquinavir, atazanavir, and amprenavir) salvage regimens [189, 190, 192, 193].
The findings of ultrasound evaluation of the kidneys may be normal; however, echogenic kidneys that are large for the patient's age and height may be seen at early and late stages of HIVAN [204]. Compared with adults, more-frequent screening is required for children because of the laboratory changes associated with growth and development.
Referral to a pediatric nephrologist is warranted for persistent significant proteinuria (grade >1+ by urine dipstick analysis or protein-to-creatinine ratio >0.2 for 3 specimens), persistent microscopic hematuria, gross hematuria in the absence of urinary tract infection, edema, hypertension, recurrent urinary tract infections, electrolyte abnormalities, persistent metabolic acidosis, or elevated blood urea nitrogen or creatinine levels.
Because data concerning treatment of HIVAN in children are lacking, therapeutic strategies should mirror those used for adult patients.
There is a great need for well-designed, prospective studies evaluating the natural history of kidney diseases in HIV-infected patients in both the adult and the pediatric populations.
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Kidney function is abnormal in up to 30% of HIV-infected patients, AIDS-related kidney disease has become a relatively common cause of end-stage renal disease (ESRD) requiring dialysis, and kidney disease may be associated with progression to AIDS and death [1-4]. Therefore, assembled clinical experts in this field have reviewed the available literature and have offered the following recommendations, many of which are extrapolated from research and clinical guidelines [5] involving the general population with kidney disease.
Blood pressure should be controlled, with the initial preferential use of angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers for those patients with proteinuria (B-II); however, calcium channel blockers should be avoided in treating patients receiving protease inhibitors (D-II).
HAART should not be withheld from patients simply because of the severity of their renal dysfunction (B-III).
The evidence for these guidelines was collected using MEDLINE searches of the relevant literature and reviews of pertinent abstracts (all in the English language) presented at both major infectious diseases and nephrology society meetings from January 2000 through February 2004.
Screening for early stages of CKD, therefore, requires measurement of urinary albumin-to-creatinine or protein-to-creatinine ratios. The incident number of patients with HIVAN undergoing dialysis each year increased through 1995, when 939 patients with HIVAN initiated dialysis. Likewise, renal laboratory abnormalities were associated with higher hospitalization rates (adjusted relative risk, 1.5) [54].
Although all decisions, including the timing of referral, should be made on a case-by-case basis, indications for such referral include abnormal kidney function, declining kidney function, or proteinuria [5]. Native arteriovenous fistulae are the preferred types of access because of excellent patency once established and lower complication rates, compared with those associated with other access options.
The largest series studied 39 HIV-infected patients receiving peritoneal dialysis and found a higher overall risk of peritonitis and more cases of peritonitis attributed to pseudomonas species and fungi than in other patients with ESRD [49, 69]; these studies were performed prior to the availability of HAART. Furthermore, a recent analysis of the USRDS confirmed that mortality in patients receiving cadaveric kidneys in the HAART era had improved dramatically, although black patients tended to be underrepresented [89]. Before therapy, underlying infection should be actively ruled out (B-III) and would be a contraindication for immunosuppressive therapy. Although reduced dosing of several antiretrovirals is advised for the patient with renal dysfunction, it should be noted that there is little clinical evidence that this actually prevents the development of toxicities while maintaining full virologic efficacy. Because the nucleoside and nucleotide reverse-transcriptase inhibitors (NRTIs) are primarily excreted by the kidneys, reduced dosage is required in those with impaired renal function, especially for drugs like didanosine and stavudine, which require further reduction because their pharmacokinetics are influenced by weight.
Furthermore, the NNRTIs and PIs have high molecular weights and are excreted into the urine in low amounts. Another 34 children had HIVAN, defined according to the clinical criteria of persistent proteinuria plus changes in radiographic or scintigraphic findings consistent with the diagnosis. FSGS denotes a poor prognosis, with rapid progression to ESRD within 1 year after presentation. As in adults, experimental evidence had suggested a direct role for HIV infection in renal pathogenesis of childhood HIVAN [217, 218].
The applicability and the efficacy of these guidelines in managing anemia in patients with HIV infection and CKD have not been addressed.
Studies of consecutively evaluated patients with evidence of renal disease that compare histological and clinical diagnoses would be invaluable. Click the links to see what we had to say.Feel free to comment on any of these books to tell your opinions of them too.
Because HIV caregivers commonly manage all aspects of treatment for their patients, these clinicians are in the unique and important position to identify those patients at risk for renal disease and implement potentially preventative and therapeutic strategies. These guidelines address the clinical issues involved in both adults and children with HIV-related renal diseases and are written for those providing inpatient and outpatient care for these patients and for the patients themselves. Addition of ACE inhibitors or angiotensin receptor blockers (ARBs) should be considered in treating both adult and pediatric patients with HIVAN if HAART alone does not result in improvement of renal function (B-II).
The evidence was graded using the Infectious Diseases Society of America-United States Public Health Service system for rating recommendations in clinical guidelines (table 1). These "spot" quantitative urine measurements of abnormal glomerular function are accurate, correlate with 24-h urine measurements, and avoid the inconvenience and difficulty in collection of timed urine specimens in clinical practice [10]. Although male sex has also been reported as a risk factor [28, 35], the incidence of HIVAN in black women is increasing proportionately to the escalating rate of HIV infection in this group [26, 40, 41], strongly suggesting that HIVAN is not sex-specific. A recent report from the Women's Interagency HIV Study Cohort further elucidated that proteinuria and elevated serum creatinine levels have been associated with greater mortality both before and after initiation of HAART [4].

Studies have shown that thrombus-free survival for native arteriovenous fistulas in HIV-positive patients is comparable to that reported for HIV-negative patients, and infection rates associated with fistulas are lower than those associated with synthetic grafts [72-74].
However, surprisingly high rates of acute and chronic rejection have been observed among HIV-infected kidney transplant recipients, with uncertain etiology at this time [88, 90]. For instance, lamivudine given in normal doses to patients with renal insufficiency does not seem to cause any obvious toxicities [119, 154]. Furthermore, because the medications in this class are neither tightly protein-bound nor have a high molecular weight, they may be easily removed by dialysis. These empirical findings suggest that dose adjustment for NNRTIs and PIs in patients with CKD is not required, although little data are available to support this general conclusion. Of note, trimethoprim and pyrimethamine reduce renal secretion of creatinine and may subsequently cause elevation of the serum creatinine level even without actual decrement in renal function; in this situation, the clinician is advised to estimate creatinine clearance using a 24-h urine collection (rather than an estimating formula) to make decisions regarding dose adjustments. It is postulated, although not proven, that ritonavir blocks the MRP-2 transporter on the apical side of the kidney proximal tubule, and thus prevents excretion of intracellular tenofovir into the urine [189].
Of these 34 children, the nephrotic syndrome developed in 7 (21%), and 14 (42%) progressed to chronic renal insufficiency. There is a high mortality rate associated with the FSGS diagnosis, with cause of death usually unrelated to renal disease [204]. Therefore, treatment goals include reduction of HIV replication to slow progression of renal disease, although studies evaluating the use of HAART or angiotensin-converting enzyme inhibitors in children with HIV-related renal diseases have not been reported.
Measurements of iron indices are complicated in HIV-infected patients, especially because levels of ferritin, which is an acute-phase protein, are often elevated in patients with HIV infection.
It is a no nonsense plan to get out of debt (if you have that problem) and build wealth and security for your family. The reader will find several terms in the medical literature that are used interchangeably and often lack precision, such as "chronic renal failure" or "chronic renal insufficiency." The National Kidney Foundation has endorsed the term "chronic kidney disease (CKD)," defined as evidence of kidney damage that persists for >3 months [5]. A simplified MDRD equation [8] that does not rely on albumin levels or weight is also highly accurate.
Increasing evidence implicates direct intrarenal HIV infection and expression of its genes in the pathogenesis of HIVAN [14-17]. From 1985 through 2000, the percentage of centers that reported providing dialysis for patients with HIV infection increased from 11% to 37%.
This salutary effect on the incidence of ESRD secondary to HIVAN likely reflects changes in the natural history of HIV disease consequent to the use of HAART.
A large series of patients with HIVAN (n = 102) confirmed that black race is a major risk factor for the presence of HIVAN but suggests that sex, risk factors for HIV acquisition, and CD4+ lymphocyte count at the time of diagnosis are not as significant as previously described [42].
Such studies predominantly reflected the clinical course of patients with advanced HIV disease who often had other opportunistic diseases. In this study, although proteinuria was positively associated with a risk of AIDS-defining illness in the pre-HAART era, elevated serum creatinine levels remained a predictor of AIDS-defining illness in the HAART era [4]. Although no studies have examined the utility of systematic screening for early kidney disease in preventing progression of renal dysfunction in HIV-infected patients, there is evidence that early treatment of CKD is beneficial [15, 52, 57-61]. In patients with evidence of CKD, imaging of the kidneys via ultrasound or other modality may provide information on the presence of stones, extrarenal and intrarenal lesions, and kidney size. Because clinical diagnosis on the basis of markers such as CD4+ cell count, HIV RNA level, and degree of proteinuria may not predict histological diagnosis in HIV-infected patients [20, 36] and because treatment options and prognosis may be influenced by the actual histological diagnosis [19], renal biopsy is recommended whenever feasible.
Renal replacement therapy can be safely delivered to HIV-infected patients by adhering to the following CDC recommendations [70].
Patients may need tunneled cuffed catheters for hemodialysis until maturation of the native arteriovenous fistula. HIV has been identified in peritoneal dialysate fluid, which should be handled as a contaminated body fluid [76]. Transplantation had not been widely available to this population until recently because of the potential risks of immunosuppression in the context of HIV disease and HIV-associated mortality itself.
A National Institutes of Health-funded, multicenter study of the safety and efficacy of kidney and liver transplantation in HIV-infected patients is expected to enroll patients through 2007 and to have a follow-up period of 2-5 years. Several reports have suggested limited benefits in renal outcomes associated with zidovudine monotherapy [59, 91, 92] and more-substantial benefits associated with the use of HAART [15, 57, 93-96].
Its potentially beneficial effects may be related to improved renal hemodynamics, reduced proteinuria, or cytokine modulation.
Periodic monitoring of renal function and pyuria should be performed during the first 6 months of indinavir therapy and biannually thereafter (B-II), although routine screening for crystalluria is not warranted unless there is a suspicion of nephrolithiasis (B-II).
Therefore, NRTIs in general should be administered after dialysis (although extra dosing to supplement the potential loss during dialysis is usually not required). Nevirapine and indinavir, however, do not fully share the drug properties of the other NNRTI and PI medications. If dapsone is chosen for Pneumocystis prophylaxis in patients requiring hemodialysis, the dose should be adjusted to 50 mg po bid, with at least 1 of the doses given after dialysis (David P.
Amphotericin B, cidofovir, foscarnet, pentamidine, and high-dose acyclovir have known nephrotoxic potential and should be administered under close supervision. Although it is mainly metabolized (80%) in the liver, its pH-based solubility in urine makes renal excretion extremely important.
The higher concentration of tenofovir that results may then cause proximal tubule necrosis and denuding of the basement membrane. Among subjects in the PACTG database, 44 patients, most of whom were black, had diagnoses consistent with HIV nephropathy. The severity of HIVAN correlated with persistently high viral loads, although 1 patient developed overt HIVAN despite good viral control (C.D.
In one report, the median time from clinical detection of nephropathy to severe renal failure was 9 months (range, 1-27 months) [205].
The degree of proteinuria may vary from minimal to nephrotic-range proteinuria [204], with associated clinical findings of edema and the full nephrotic syndrome.
Although it is at times inaccurate, estimation of GFR in clinical practice can be easily performed with use of a formula derived by Schwartz et al.
Drugs that require elimination by the kidney should have dose adjustments made to avoid toxicities in all patients with renal insufficiency, using data for adults as a guide.
In the 15 children with nephrotic syndrome described above, 13 were treated with steroid therapy, with no response. In HIV-infected patients, several reports of osteopenia and osteoporosis have been described in the literature [225].
The development of protective antibodies and the duration of this protection is likely to be short because of decreases in the levels of these antibodies [235]. I'll write a full review later, I promise. I'd also like to open up the floor to let others suggest the titles they think are some of the best personal finance books and books on money management and budgeting. After all, I can't read everything or know all the good ones, so what are your faves?
Select it and click on the button to choose it.Then click on the link if you want to upload up to 3 more images. As shown in table 2, the severity of CKD is graded according to renal function, on the basis of estimates of either the creatinine clearance (calculated using the Cockcroft-Gault equation) [6] or the GFR (calculated using the modification of diet in renal disease [MDRD] equation) [7].
These equations have not been validated for the HIV-infected population; therefore, there is no absolutely preferred equation to use consistently among patients with HIV infection. The currently available epidemiological data may be limited by potential biases introduced through selection of patients following referral to a nephrologist or by the performance of either biopsy or autopsy. As screening for HIV became more routine and resulted in earlier detection, several groups reported improved survival among HIV-infected dialysis patients beginning in the early 1990s [22, 45-49]. The clinical evaluation of patients at increased risk for CKD includes assessment of markers of kidney damage, such as proteinuria, kidney function, and blood pressure. Although HIVAN is associated with large echogenic kidneys [63], this relationship is not sufficiently predictive of HIVAN to use as a diagnostic tool. Prior to the use of effective antiretroviral therapy, case reports and series reported mixed outcomes in HIV-infected renal transplant recipients, including both rapid HIV progression and long-term survival [78, 79]. The exception to this is abacavir, which has relatively low urinary excretion, is more tightly protein-bound, and has more-extensive hepatic metabolism. Because of nevirapine's relatively low molecular weight and protein-binding fraction, it has been suggested that dialysis may remove substantial amounts of this drug [133, 134]. Amphotericin B causes renal effects in up to 80% of treated patients, including hypokalemia, bicarbonaturia, renal tubular acidosis, decreases in renal erythropoietin and anemia, and elevations in the serum creatinine level. Renal toxicity occurs with accumulation of these compounds in the proximal tubule and appears to be concentration dependent [181].

Although the underlying mechanisms triggering bone loss in HIV-infected patients are not completely defined, traditional risk factors, HIV infection itself, HIV-associated fat redistribution, antiretroviral therapy for HIV infection, and increased production of proinflammatory cytokines (such as TNF and IL-6) may have roles in osteoclast activation and resorption [225-230]. Among outpatients, ARF is commonly caused by drug-specific renal toxicities (see "Renal Effects of Commonly Used Medications in HIV Care") and prerenal states associated with dehydration. There is no evidence in the literature that suggests a definitive way other than renal biopsy to distinguish patients with HIVAN from patients with diseases other than HIVAN.
Even in patients with normal kidney function, the presence of proteinuria may indicate early kidney disease. With the dramatic reductions in HIV-associated morbidity and mortality observed since the availability of HAART, the safety of immunosuppression in this population has become the more pressing concern. An additional renal biopsy has demonstrated dramatic improvements in renal histological findings in association with HAART [15].
In patients who develop indinavir nephrolithiasis, it would be reasonable to restart indinavir therapy once rehydration is achieved (B-III).
Therefore, dosing adjustment for this drug in patients with renal insufficiency is not necessary, although it should still be administered after hemodialysis to minimize drug loss [120]. Alternatively, the association between the use of tenofovir with ritonavir-boosted protease inhibitors and Fanconi syndrome may simply be a marker of patients in deep salvage therapy with more longstanding HIV infection that could, in general, lead to a higher incidence of nephropathy. All children with AIDS and nephropathy (n = 16) died during the 10-year study period, with a mean survival time of 9.5 months after renal disease was diagnosed. Schwartz and coworkers devised a useful graph (figure 2) for mean normal creatinine values by age, based on applying this formula to a large population of healthy children [213]. HIV-infected patients have been reported to have low baseline and maximal secretion of parathyroid hormone and 1,25-dihydroxyvitamin D3 levels [228, 231, 232].
Several reports have suggested that antibody response to vaccination for hepatitis B is impaired in HIV-infected patients [236, 237]. More pharmacokinetic evaluations of the proper dosing of antiretroviral agents in both children and adults should also be performed.
Because studies of medications in renal failure have traditionally used the Cockcroft-Gault equation, it would be appropriate to use this estimating formula in deciding on dosage. As HIVAN predominantly affects black persons, it is not surprising that most HIV-infected ESRD patients (87.8%) are African American [26]. Blockade of the renin-angiotensin system may have specific benefits in those hypertensive patients with proteinuria (see the subsection "ACE inhibition" in the section Management).
Unfortunately, after several years of HAART therapy, some patients eventually progress to ESRD through uncertain mechanisms [97]. Indinavir's plasma protein-binding fraction is also lower than those of other PIs, and 10% of unchanged drug is excreted in the urine. Cidofovir causes dose-dependent nephrotoxicity (including glycosuria, bicarbonaturia, phosphaturia, polyuria, and nephrogenic diabetes insipidus) that is reduced by coadministration of intravenous hydration and probenecid, which prevents the active uptake of cidofovir at the basolateral surface of the proximal tubule [157]. They also reported symptomatic patients with crystalluria, dysuria, and urgent urination; asymptomatic crystalluria occurred in 20% of indinavir-treated patients. However, at the lower dose approved for the treatment of hepatitis B virus infection, renal failure rates appear low [183, 184].
This is supported by a cohort study [188] that suggests that renal toxicity occurs primarily in patients with more-severe HIV disease and longer overall antiretroviral treatment duration.
Thirty-two (70%) of 56 children without nephropathy were alive at the end of the study period.
Parathyroid cells have been found to express protein recognized by antibodies directed against CD4+ cells, suggesting that parathyroid cells may be infected with HIV and with subsequent impairment of parathyroid hormone release. Some of these questions are currently being addressed by the PACTG and the Adult AIDS Clinical Trials Group, and they will hopefully lay the foundation for further research in this emerging field. HIVAN had a stronger association with black race than with any other cause of renal failure except sickle cell anemia. Calcium channel blockers of both the dihydropyridine and nondihydropyridine classes should be used with caution because of their potential interaction with protease inhibitors, which can result in hypotension and possibly in conduction delays [67].
It should also be noted that the lower drug dosing recommendations for tenofovir are intended for patients with stable CKD and not for those whose renal function deteriorates as a result of tenofovir-related nephrotoxicity or some other acute insult.
However, several case reports have demonstrated no appreciable change in indinavir's pharmacokinetic parameters, although it may be prudent to initiate hemodialysis at the end of a dosing interval [140, 141]. Pyuria (but not necessarily crystalluria) secondary to treatment with indinavir has been associated with gradual loss of renal function unrelated to obstructive symptoms [165]. Tenofovir was not associated with higher rates of renal failure in initial treatment studies [185, 186], although patients with preexisting renal dysfunction were not included. FSGS was the most common renal lesion in this series, diagnosed in 6 of 13 children who underwent renal biopsy [206]. One series that described 6 pediatric patients with HIVAN reported that 15 patients presented with nephrotic-range proteinuria, and 1 presented with mild proteinuria. Low 1,25-dihydroxyvitamin D3 levels are associated with low CD4+ lymphocyte counts, advanced HIV infection, and higher TNF-a levels. Risk factors include low lean-body mass, indinavir regimens of ⩾1000 mg administered twice daily, concomitant use of trimethoprim-sulfamethoxazole [163, 166], and coinfection with either hepatitis B or C [167, 168].
Two of these patients had hematuria in addition to proteinuria, and 1 patient received a diagnosis of renal tubular acidosis [206].
Renal toxicity is the major side effect of foscarnet use and can be reduced with intravenous saline or 5% dextrose solution hydration before and during slow infusion. Environmental conditions, including temperature, atmospheric pressure, and humidity, affect the risk of developing indinavir nephrolithiasis [163, 169]. Risk factors in this study included preexisting renal dysfunction, low body weight, and long duration of tenofovir use [194].
Of 15 children with nephrotic syndrome who were followed-up from 1984 through 1990 in Brooklyn, New York, 30% experienced ESRD within 8 months after diagnosis, with successful peritoneal dialysis performed for 3 children. Renal disease in children who are HIV positive may be "classic" HIVAN, but it may also include fluid and electrolyte abnormalities, urinary tract infections, renal tubular acidosis, ARF, treatment-related nephrotoxicity, infiltrative diseases of the kidney, hemolytic uremic syndrome, or IgA nephropathy [204, 209]. Foscarnet administration is associated with hypocalcemia, hypophosphatemia, hyperphosphatemia, hypomagnesemia, and hypokalemia. Ritonavir-boosted indinavir regimens may lead to higher risk of nephrolithiasis, with higher indinavir peak concentrations being associated with development of urologic symptoms [170], as well as to rhabdomyolysis-induced renal failure [171]. Prior exposure to high-dose adefovir dipivoxil does not appear to be associated with an increased risk of nephrotoxicity [187].
Although data on bone disease in patients with CKD and HIV infection is not available, it is known that HIV-infected patients with CKD develop complications of altered calcium and phosphate metabolism similar to HIV-negative patients [233].
Impaired baseline renal function, low total serum calcium level, and underlying CNS conditions were risk factors associated with seizures during foscarnet treatment.
In addition, the highest incidence of urologic symptoms occurred during the first 6 months of indinavir treatment. Determintion of creatinine clearance and measurement of electrolytes are recommended at baseline, 2-3 times per week during induction therapy, and every 1-2 weeks during maintenance therapy. Fortunately, most cases of ARF secondary to indinavir resolve with discontinuation of the drug. On suspicion of indinavir nephrotoxicity, urine should be inspected for the presence of crystals and pyuria [172].
Indinavir has also been associated with hypertension [173], renal atrophy [174], interstitial nephritis [175, 176], development of renal failure associated with fever and rash [177], and persistent leukocyturia with renal failure [178, 179]. A daily intake of at least 1.5 liters of water usually prevents stone formation, especially in those with the risk factors outlined above. There is little risk of recurrent nephrolithiasis or ARF associated with dehydration if indinavir therapy is restarted once rehydration is achieved.
Indinavir should not be withheld in patients with severe kidney disease for fear of increased risk of nephrolithiasis because little of the drug will actually reach the collecting system.

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