HIV/AIDS Skepticism

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

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“.

4 Responses to “HAART denialism, contd.”

  1. mykoolaidtastesfunny said

    Hi Dr Bauer…could you comment on this study?

    J Clin Virol. 2010 Feb;47(2):131-5. Epub 2009 Dec 16.

    The prognosis of highly active antiretroviral therapy (HAART) treated HIV infected patients in Serbia, related to the time of treatment initiation.

    I’ve commnented before and I don’t believe in Gallo’s virus so I’m just wanting your critique. Someone showed this to me as evidence of how awesome HAART is. It looks like rubbish to me because there was nobody not taking the drugs so how could anyone compare taking vs not taking them but I’m not a scientist. It claims that “viral load” counts shows increased health and lifespan. Would this refute the 2006 Lancet study which showed the exact opposite?

    • Henry Bauer said

      Soon. Too many urgent things to attend to. As Jack Good liked to say (and bemoan), the urgent drives out the important

    • Henry Bauer said

      Yes, I think that article is BS, in large part because other articles tell different stories and the authors here admit some of the flaws. As you noted, no control group. The usual reliance on viral load and CD4 counts as measures of favorable outcome, instead of clinical condition. The ESTIMATION of survival times.
      A cursory read persuades me that it’s not worth analyzing in detail.

  2. mykoolaidtastesfunny said

    Thank you Dr Bauer. I haven’t been educated in the jargon but I figured it was rubbish based on everything else I’ve read. You don’t have to be educated in Latin to know the Bible is full of contradictions and general rubbish.

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