HIV/AIDS Skepticism

Pointing to evidence that HIV is not the necessary and sufficient cause of AIDS

Posts Tagged ‘HAART causes kidney disease’

HAART denialism, contd.

Posted by Henry Bauer on 2010/12/06

That ART causes kidney disease is obfuscated by assertions that “HIV” itself does so. There are even claims that introduction of HAART was associated with a decrease in “incidence and occurrence of renal disease” [Mocroft et al., “Estimated glomerular filtration rate, chronic kidney disease and antiretroviral drug use in HIV-positive patients”, AIDS, 24 [2010] 1667-78; see “Kidney-disease denialism (a special case of HAART denialism)”, 2010/11/20]. The source references for that claimed decrease are Ross & Klotman, “Recent progress in HIV-associated nephropathy”, Journal of the American Society of Nephrology 13 (2002) 2997-3004 and Weiner, Goodman & Kimmel, “The HIV-associated renal diseases: current insight into pathogenesis and treatment”, Kidney International 63 (2003) 1618-31. I’ve now read both.
Unwary readers might interpret the claim of a decrease as a steady drop, but neither of these sources bears out that claim. There was a small drop in incidence around 1996-97, but this was followed by either no decrease or an actual increase:


Overall “HIV disease” mortality dropped by about half in 1996-97 when HAART was introduced, as shown in Ross & Klotman, Figure 2. I’ve discussed this in detail before [HAART saves lives — but doesn’t prolong them!?, 17 September 2008]. Halving of mortality in the space of about a year cannot be ascribed to antiretroviral action, because that would only allow the immune system to regenerate slowly; on the other hand, cessation of highly toxic monotherapy (chiefly AZT) could bring a rapid decline in mortality: stop taking poison and your chances of dying decrease dramatically and quickly.
The data from Ross & Klotman and from Weiner, Goodman & Kimmel show that after the initial decline in fatal renal disease, when monotherapy was replaced by HAART, there has been no continuing decline: HAART continues to cause kidney disease, just slightly less effectively or more slowly than AZT alone.
Mocroft et al. were misleading quite seriously by citing these sources as reporting HAART-associated decline in kidney disease. Presuming that they were not misleading deliberately, at the very least they demonstrated themselves to be untrustworthy when citing sources.

So much for the false claim that HAART reduced the incidence of kidney disease. On to the false claim that kidney disease is “HIV-associated” rather than ARV-associated.

Weiner et al. speak of “intrinsic” acute renal failure in “patients with HIV infection”, and cite several sources for the claim that “HIV infection” has been found to be associated with a variety of “nephrological syndromes responsible for both acute and chronic renal failure”. Their two most recent sources date from 1990. One of them — Seney, Burns, & Silva, American Journal of Kidney Disease, 16 (1990) 1-13 — does not say “HIV”-associated, its title is “Acquired immunodeficiency syndrome and the kidney”, and the text describes work with AIDS patients. The other is a review that draws on 115 sources and notes that “HIV-associated nephropathy” was formerly termed AIDS-associated nephropathy [Glassock et al., “Human immunodeficiency virus (HIV) infection and the kidney”, Annals of Internal Medicine, 112 (1990) 35-49]. In point of fact, all the reviewed observations were derived from patently ill AIDS patients.
For anything to be properly described as “HIV-associated”, it should be proven to be associated with being “HIV-positive”, not with being an AIDS patient.

According to Glassock et al., hyponatremia (too little sodium) is the most common electrolyte or fluid abnormality associated with AIDS or AIDS-related complex; found, in other words, in people who were clinically ill, with Pneumocystis carinii (PCP) in a high proportion of the studied cases. Possible causes of nephrotoxicity include such drugs as pentamidine, which was a common treatment for and prophylaxis against PCP.
The peculiar distribution of this “HIV-associated” nephropathy “has suggested to some investigators that HIV infection is not responsible, directly or indirectly, for the renal damage”. That conclusion does seem natural, even obvious, given that 90% of the cases were in blacks. Among nearly 3000 AIDS patients in New York and Miami, nearly 180 (6%) had advanced kidney disease, the risk factors being black and abusing drugs intravenously; whereas among 1000 largely white gay men in San Francisco, only 13 (1.3%) had advanced kidney disease, and of those 13 the 3 most affected (on chronic dialysis) were black. If “HIV” were the cause of AIDS and of the kidney disease, the significantly lower rate in San Francisco and the extraordinary racial disparity would be a real mystery.
The ultimate treatment for renal failure is kidney transplant. Healthy immune systems reject transplants, and immunosuppressive therapy is needed to avoid that. Since “HIV” suppresses the immune system, kidney transplanting in “HIV-associated nephropathy” should be less problematic in terms of rejection; yet it isn’t:
“Despite the profound immunosuppression intrinsic to the HIV-infected patient, there remains such a remarkably intact capacity to respond to allogenic stimulation that acute rejection is an ever-present fear in HIV-infected transplant patients”; while the fear of opportunistic infections in “HIV-positive” patients “is exaggerated severalfold”.

Clearly, this review not only speaks against “HIV-associated nephropathy” as being HIV-caused, it also provides evidence that “HIV infection” is not associated with profound immunosuppression.
Moreover, hyponatremia, the most common electrolyte disturbance in AIDS, may be caused by stomach ailments that produce diarrhea or vomiting, plausibly in connection with intestinal dysbiosis. Here is further indirect support for the hypothesis that lifestyle-associated intestinal dysbiosis was a major factor in the AIDS outbreaks in the early 1980s.

There is no need to postulate “HIV-associated” nephropathy.

There is no need to postulate “HIV“.

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Kidney-disease denialism (a special case of HAART denialism)

Posted by Henry Bauer on 2010/11/20

Mainstreamers have perfected the ART of explaining away the toxicities of HAART even as they publish illustrations of its statistically significant toxicities. They find  that HAART causes oxidative stress even “during apparently successful HAART”, which “underline[s] HAART associated toxicity”; yet they practice HAART denialism by calling it “life-saving”.
They know that protease inhibitors cause lipodystrophy, but practice denialism by calling it “HIV-associated” lipodystrophy.
They know that HAART causes kidney disease, but practice denialism by calling it “HIV-associated nephropathy”, underscoring how well established this is supposed to be by giving it an acronym, HIVAN (Mocroft et al., “Estimated glomerular filtration rate, chronic kidney disease and antiretroviral drug use in HIV-positive patients”, AIDS, 24 [2010] 1667-78):
“increasing exposure to tenofovir was associated with a higher incidence of CKD [chronic kidney disease] . . . .
Nephrolithiasis was seen in up to 27% of patients treated with indinavir [23,24] and there are numerous studies [25–29] demonstrating that tenofovir is associated with impaired kidney function . . . .”
After 24 months, 1.5% of patients on HAART had developed kidney disease, and 3% had after 36 months. Two other methods of assessing the results gave similar numbers, 0.95 and 0.88 respectively as incidence of kidney disease per year ( = 1.8-1.9% after 24 months, 2.7-3% after 35 months).
Now how could one practice denialism in the face of these statistically significant findings?
Here’s how:
“This study has demonstrated a relatively low proportion of patients developing CKD and that in addition to the traditional risk factors for renal disease, increasing exposure to tenofovir, indinavir, atazanavir and lopinavir was associated with an increased incidence of CKD” [emphasis added] —
A few percent is indeed a low percentage, though one doubts whether properly informed patients would willingly accept that high a probability of losing their kidney function.
The insertion of “in addition to the traditional risk factors” has only one purpose, to defuse the following admission that HAART kills kidneys. Those “traditional” factors include age, hypertension, and diabetes; but they are entirely irrelevant, since HAART independently kills kidneys.
The abstract practices this denialist obfuscation in its first sentence: “Chronic kidney disease (CKD) in HIV-positive persons might be caused by both HIV and traditional or non-HIV-related factors”. What the article fails to say, though, is that the work proves that HAART causes kidney disease but offers absolutely no evidence that “HIV” does.
Admittedly, some patients “at baseline” already had early signs of kidney disease; but given that “HIV” tests react poz to a wide range of disease conditions, it may well be that those individuals tested “HIV-positive” only because they already suffered from some sort of kidney problems — which “treatment” then promptly made worse.
The article’s “Introduction” lays HIV/AIDS belief on the line at once:
“HIV infection is associated with renal dysfunction, including HIV-associated nephropathy (HIVAN), immune complex kidney disease and acute renal failure [1,2], which may be associated with progression to AIDS and death [3,4]. There is increasing evidence that HIV infection of the kidneys is involved with HIVAN [5], whereas other disorders include nephropathy resulting from coinfection with hepatitis B, hepatitis C or syphilis [6,7]; diabetes or hypertension [8] and immune complex glomerulonephritis [9]”.
This is followed by remarkable claims:
“The incidence and occurrence of renal disease has decreased since the widespread introduction of combination antiretroviral therapy (cART) [10,11], with studies suggesting that cART reduces the incidence of HIVAN [12], possibly by slowing the decline in renal function [13,14]”.
I’m awaiting delivery of copies of those references 10-14, but it is curious indeed that Mocroft et al. should cite them in this manner but then, in their abstract and conclusions, point only to kidney damage done by HAART. Evidently their work has superseded and contradicted those earlier claims, yet they cite them here and do not anywhere discuss the conflict with their own findings. To have done so would, of course, have made kidney-disease denialism and HAART denialism more difficult.
The article’s final paragraph seeks to give the impression that kidney damage comes only from tenofovir:
“increasing exposure to tenofovir was associated with a higher incidence of CKD independently of other antiretroviral drugs and traditional CKD risk factors. The increase in risk of CKD was also true for indinavir and atazanavir, whereas the results for lopinavir/ r were less clear. There may be some reversibility in CKD after discontinuation of the antiretroviral drugs, but this requires confirmation in larger studies with longer follow-up”.
While the large effect of tenofovir could not be denied, the attempt to make it seem that there is some doubt about damage from the others is disingenuous, for the incidence-over-time trend is reported as positive in all of these cases, at very high statistical significance, p<0.0001 (Figure 2).
Furthermore, the suggested hope that HAART-caused kidney damage might be reversible is not supported by the earlier observation of “high risk of CKD in the group of people within 12 months of stopping tenofovir”.
The call for more research is routine, of course, and demonstrates the willingness of HIV/AIDS researchers to continue to observe, for the good of science and medicine and humanity, what happens to people who are being slowly poisoned by their “treatment”.
As of January 2009, there were well over 100 clinical trials of tenofovir (Tenofovir and the ethics of clinical trials), including as prophylaxis (Prophylaxis via organ failure and bankruptcy) against contracting “HIV”, some of them using tenofovir in a microbicide (More clinical trials in Africa; Reading HIV/AIDS numbers) despite the horrendous “side” effects that had long been known (To avoid HIV later, damage your kidneys and liver now, 19 January 2008).

Tuskegee and Guatemala were not the last examples
of Mengele-type human experimentation
by doubtless-well-intentioned medical researchers.

Posted in antiretroviral drugs, clinical trials, experts, HIV risk groups, HIV skepticism, HIV tests | Tagged: , | 7 Comments »