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  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?
“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 , whereas other disorders include nephropathy resulting from coinfection with hepatitis B, hepatitis C or syphilis [6,7]; diabetes or hypertension  and immune complex glomerulonephritis ”.
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 , 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.
This entry was posted on 2010/11/20 at 9:49 am and is filed under antiretroviral drugs, clinical trials, experts, HIV risk groups, HIV skepticism, HIV tests. Tagged: HAART causes kidney disease, tenofovir toxicity. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.