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Chronic Kidney Disease (CKD), End Stage Renal Disease (ESRD), and renal failure

Grant Genereux fixed his own Chronic Kidney Disease (CKD) by simply avoiding Poison/"Vitamin A" as much as possible in his diet (which his doctors to this day have never seen anyone else come out of this problem to return to normal kidney function like Grant did).  This connects to the fact that there is a ton of research linking hypervitaminosis A to CKD.  The two are intimately related.

Remember, that glyphosate/Roundup causes the liver to become unable to break down Poison/"Vitamin A", thus increasing/aggravating the rate of Poison/"Vitamin A" toxicity.  This is the foundation of the Unified Theory of Modern Chronic Disease.

If the above were true, we would expect the rates of chronic kidney disease to be RISING due to increased glyphosate use and Poison/"Vitamin A" everywhere, right?  Ask and ye shall receive:

For U.S. adults aged 30 to 49, 50 to 64, and 65 or older with no CKD at baseline, the residual lifetime incidence of CKD is 54%, 52%, and 42%, respectively, according to Dr. Hoerger’s research. This compares to lifetime incidences of 12.5% for breast cancer in women, 33% to 38% for diabetes, and 90% for hypertension in middle-aged men and women.

Now, on to the research evidence.  After you see all of this, it will sure seem amazing that modern medicine can't figure out what is causing this problem!  (that was sarcasm)

Implications of Hypervitaminosis A in Chronic Renal Failure

Numerous studies have shown that elevated levels of vitamin A may be found in the liver and plasma of patients with renal failure.

Hypervitaminosis A is prevalent in children with CKD and contributes to hypercalcemia

CONCLUSIONS: Hypervitaminosis A is seen in early CKD, with highest levels in children on supplemental feeds compared with diet alone. Serum retinoid levels significantly predict hypercalcemia.

Hypercalcaemia Secondary to Hypervitaminosis A in a Patient with Chronic Renal Failure

Vitamin A toxicity is a well-described medical condition with a multitude of potential presenting signs and symptoms. It can be divided into acute and chronic toxicity. Serum vitamin A concentrations are raised in chronic renal failure even with ingestion of less than the usual toxic doses. Hypercalcaemia can occasionally be associated with high levels of vitamin A but it is rare. In this report, we describe a 67- year old female patient with chronic kidney disease who was taking vitamin A supplements for approximately 10 years. The patient had worsening of her chronic kidney disease over the last years and developed chronic hypercalcaemia. Her vitamin A level was elevated with a daily intake of 7000 IU. The vitamin A supplement was stopped. A few months later, vitamin A level diminished substantially and serum calcium levels returned to normal.

[Hypercalcemia due to chronic vitamin A use by an elderly patient with renal insufficiency].

An 86-year-old woman presented with anorexia, thirst and nycturia [aka nocturia, having to pee in the middle of the night]. Laboratory results revealed a hypercalcaemia with renal failure. The patient used 1-6 vitamin A-D tablets daily (1 tablet contains 600 IU retinol palmitate and 200 IU cholecalciferol). The diagnosis was: hypercalcaemia due to chronic vitamin A ingestion. This diagnosis was supported by the finding of the elevated vitamin A concentration in the patient's serum and the exclusion of other causes of hypercalcaemia. In chronic vitamin A ingestion risk factors for vitamin A toxicity are age, body weight and renal insufficiency. The hypercalcaemia caused by chronic vitamin A ingestion is explained through the up-regulation of osteoclasts by retinol metabolites.

Note that the last bolded sentence above means that the Poison/"Vitamin A" was eating away at bone calcium, and that is how the blood calcium levels went too high (hypercalcemia).  Osteoporosis is well-linked to Poison/"Vitamin A" in other posts on this blog-forum.

[Vitamin A poisoning revealed by hypercalcemia in a child with kidney failure].

CASE REPORT: An 8 year-old boy with Alagille syndrome and chronic renal failure was admitted because of general deterioration, and bone pain. Severe hypercalcemia (3.9 mmol/L) was present. Serum phosphate, parathyroid hormone and 25 OH D3 levels were normal; 1-25 (OH)2 D3 levels were undetectable. Hypercalcemia was attributed to vitamin A intoxication, due to the administration of a mean daily dose of 12000 IU of vitamin A for at least 2 years. The diagnosis was confirmed by high plasma levels of retinol (1475 micrograms/L). Hypercalcemia only partially responded to treatment with bisphosphonates, calcitonin and dialysis with low calcium dialysate. Serum vitamin A levels remained elevated one month after vitamin A withdrawal. The boy died two months after admission from atrioventricular block.

CONCLUSION: Vitamin A administration induces a high risk of intoxication in patients with chronic renal failure. Serum vitamin A concentrations are elevated in these patients, because of decreased renal metabolism of retinol, and vitamin A supplements must be avoided.

Serum retinol, retinol-binding protein, and transthyretin in children receiving dialysis.

OBJECTIVE: We investigated the relationships of retinol (ROH), retinol-binding protein (RBP), and transthyretin (TTR) in children with end-stage renal disease (ESRD). Our hypothesis was that levels of ROH and RBP would be elevated in children with ESRD.
CONCLUSIONS: The data indicate that children with ESRD exhibit elevated levels of serum ROH, RBP, and TTR, in proportions similar to those reported in the adult ESRD literature. Further study is needed to clarify the consequences of increased ROH in uremic children.

Serum levels of vitamin A and retinol binding protein in chronic renal patients treated by continuous ambulatorial peritoneal dialysis.

Patients on dialysis had higher retinol levels than untreated patients. Retinol levels were found to be correlated with RBP levels.

Chronic Kidney Disease Alters Vitamin A Homeostasis via Effects on Hepatic RBP4 Protein Expression and Metabolic Enzymes

We measured retinoid and RBP4 concentrations in plasma and urine from 55 adult patients with CKD and 21 matched healthy subjects. RBP4 and retinol levels were increased approximately twofold in patients with CKD, with a negative correlation between plasma retinol and eGFR (p = 0.006) and plasma RBP4 and eGFR (p = 0.0007). RBP4 renal clearance was higher in patients with CKD than healthy subjects but not associated with eGFR. Circulating concentrations of atRA increased and concentrations of 13cis-RA decreased in subjects with CKD with no change in RA-to-retinol ratio. Increases in circulating retinol, RBP4, and atRA may be due to increased hepatic RBP4 synthesis, retinyl ester hydrolysis, and/or hepatic secretion of RBP4-retinol.

Isoforms of Retinol binding protein 4 (RBP4) are increased in chronic diseases of the kidney but not of the liver

The levels of retinol-binding protein 4 (RBP4) – the carrier protein for Vitamin A in plasma – are tightly regulated under healthy circumstances. The kidney, the main site of RBP4 catabolism, contributes to an elevation of RBP4 levels during chronic kidney disease (CKD)
RBP4 isoforms and levels were highly increased in CKD patients compared to controls (P < 0.05)

If you have this issue, make sure to ask your nephrologist if they know anything about it, and WHY they haven't thoroughly investigated all aspects of your Poison/"Vitamin A" levels.  You will likely be quite disappointed in the response.


Dr. Garrett Smith, the "Nutrition Detective"
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