MESO-Rx
Anabolic Steroids
Anabolic Steroids & Kidney
- Thread starter Michael Scally MD
- Start date
gearwolf
Member
As someone with a congenital leptin deficiency that actually eats ~1000g on some of my worst days, which is still "only" ~4000 calories of protein, and accounting that my gut microbiome is somewhat adapted to this intake, I still spend most of those days on the shitter, so I highly doubt those numbers as well unless they were served proteins to the bathroom all day.
RoidmeDangerfield
Member
According to this study, it seems my theory about blood viscosity might be correct:
The Relationship Between Plasma Whole Blood Viscosity and Cardiovascular Events in Patients With Chronic Kidney Disease. - PubMed - NCBI
Although it's not making any solutions on what to do to improve the situation I'm wondering if regular therapeutic blood draws would help to keep blood viscosity levels down; which in turn helps reduce stress on the kidneys.
I also notice that when I get my therapeutic blood draw my prehypertensive blood pressure goes down to a very good level.
The Relationship Between Plasma Whole Blood Viscosity and Cardiovascular Events in Patients With Chronic Kidney Disease. - PubMed - NCBI
Although it's not making any solutions on what to do to improve the situation I'm wondering if regular therapeutic blood draws would help to keep blood viscosity levels down; which in turn helps reduce stress on the kidneys.
I also notice that when I get my therapeutic blood draw my prehypertensive blood pressure goes down to a very good level.
Effects of Bodybuilding Supplements on The Kidney
Background: The incidence of kidney diseases among bodybuilders is unknown.
Methods: Between January 2011 and December 2019, the Iraqi Kurdistan 15 to 39 year old male population averaged 1,100,000 with approximately 56,000 total participants and 25,000 regular participants (those training more than 1 year). Annual age specific incidence rates (ASIR) with (95% confidence intervals) per 100,000 bodybuilders were compared with the general age-matched male population.
Results: Fifteen male participants had kidney biopsies. Among regular participants, diagnoses were: focal segmental glomerulosclerosis (FSGS), 2; membranous glomerulonephritis (MGN), 2; post-infectious glomeruonephritis (PIGN), 1; tubulointerstitial nephritis (TIN), 1; and nephrocalcinosis, 2. Acute tubular necrosis (ATN) was diagnosed in 5 regular participants and 2 participants training less than 1 year.
Among regular participants, anabolic steroid use was self-reported in 26% and veterinary grade vitamin D injections in 2.6%.
ASIR for FSGS, MGN, PIGN, and TIN among regular participants was not statistically different than the general population. ASIR of FSGS adjusted for anabolic steroid use was 3.4 (- 1.3 to 8.1), a rate overlapping with FSGS in the general population at 2.0 (1.2 to 2.8). ATN presented as exertional muscle injury with myoglobinuria among new participants.
Nevertheless, ASIR for ATN among total participants at 1.4 (0.4 to 2.4) was not significantly different than for the general population at 0.3 (0.1 to 0.5). Nephrocalcinosis was only diagnosed among bodybuilders at a 9-year cumulative rate of one per 314 vitamin D injectors.
Conclusions: Kidney disease rates among bodybuilders were not significantly different than for the general population, except for nephrocalcinosis that was caused by injections of veterinary grade vitamin D compounds.
Ali AA, Almukhtar SE, Sharif DA, Saleem ZSM, Muhealdeen DN, Hughson MD. Effects of bodybuilding supplements on the kidney: A population-based incidence study of biopsy pathology and clinical characteristics among middle eastern men. BMC Nephrol. 2020;21(1):164. Published 2020 May 6. doi:10.1186/s12882-020-01834-5 Effects of bodybuilding supplements on the kidney: A population-based incidence study of biopsy pathology and clinical characteristics among middle eastern men
Background: The incidence of kidney diseases among bodybuilders is unknown.
Methods: Between January 2011 and December 2019, the Iraqi Kurdistan 15 to 39 year old male population averaged 1,100,000 with approximately 56,000 total participants and 25,000 regular participants (those training more than 1 year). Annual age specific incidence rates (ASIR) with (95% confidence intervals) per 100,000 bodybuilders were compared with the general age-matched male population.
Results: Fifteen male participants had kidney biopsies. Among regular participants, diagnoses were: focal segmental glomerulosclerosis (FSGS), 2; membranous glomerulonephritis (MGN), 2; post-infectious glomeruonephritis (PIGN), 1; tubulointerstitial nephritis (TIN), 1; and nephrocalcinosis, 2. Acute tubular necrosis (ATN) was diagnosed in 5 regular participants and 2 participants training less than 1 year.
Among regular participants, anabolic steroid use was self-reported in 26% and veterinary grade vitamin D injections in 2.6%.
ASIR for FSGS, MGN, PIGN, and TIN among regular participants was not statistically different than the general population. ASIR of FSGS adjusted for anabolic steroid use was 3.4 (- 1.3 to 8.1), a rate overlapping with FSGS in the general population at 2.0 (1.2 to 2.8). ATN presented as exertional muscle injury with myoglobinuria among new participants.
Nevertheless, ASIR for ATN among total participants at 1.4 (0.4 to 2.4) was not significantly different than for the general population at 0.3 (0.1 to 0.5). Nephrocalcinosis was only diagnosed among bodybuilders at a 9-year cumulative rate of one per 314 vitamin D injectors.
Conclusions: Kidney disease rates among bodybuilders were not significantly different than for the general population, except for nephrocalcinosis that was caused by injections of veterinary grade vitamin D compounds.
Ali AA, Almukhtar SE, Sharif DA, Saleem ZSM, Muhealdeen DN, Hughson MD. Effects of bodybuilding supplements on the kidney: A population-based incidence study of biopsy pathology and clinical characteristics among middle eastern men. BMC Nephrol. 2020;21(1):164. Published 2020 May 6. doi:10.1186/s12882-020-01834-5 Effects of bodybuilding supplements on the kidney: A population-based incidence study of biopsy pathology and clinical characteristics among middle eastern men
shaquille_oatmeal_777
Member
Hi Michael, do you have any views on thymoquinone (TQ)? It's one of three phytochemicals in black seed oil. The other two are Thymohydroquinone and Thymol. You'll find research on the health benefits of TQ in a wide range of areas in the human body, such as in reversing acute renal disease, chronic liver disease issues, and other cardiovacular issues as well. I find very few people know of its existence and the positive impact it has on the human body. Anyhow, I was just reading your post here regarding AAS and the implications on kidneys and wondering if you've come across TQ in your research and what your views are, if any!? Thank you!
Simple Summary on Black Seed Oil: The Powerful Medicinal Oil with Virtually No Side Effects
Simple Summary on Black Seed Oil: The Powerful Medicinal Oil with Virtually No Side Effects
A yearslong push to remove racist bias from kidney testing gains new ground
Push to remove racist bias from kidney testing gains new ground
For years, physicians and medical students, many of them Black, have warned that the most widely used kidney test — the results of which are based on race — is racist and dangerously inaccurate. Their appeals are gaining new traction, with a wave of petitions and papers calling renewed attention to the issue.
In recent weeks, physicians and medical students at a handful of prominent universities have called on their administrations to end the use of race-based kidney testing, pointing to such changes at Beth Israel Deaconess Medical Center in 2017 and at Mass General Brigham and the University of Washington earlier this summer.
On the heels of those petitions, as well as a widely circulated New England Journal of Medicine analysis of the kidney test and other medical tools that are biased against Black patients, the National Kidney Foundation and the American Society of Nephrology announced this month that they will convene a task force to evaluate the use of race in kidney testing. https://www.nejm.org/doi/full/10.1056/NEJMms2004740
“[Science] has been a conspirator of racism since the genesis of racism. And it is our duty as physicians to be keenly aware and critical of that history, and how we still operate within it despite our best intentions,” said Paloma Orozco Scott, a medical student who co-authored a petition to Mount Sinai calling to end the use of race as a factor in the test.
The test — which measures what’s known as estimated glomerular filtration rate, or eGFR — has historically considered four factors: age, gender, race, and levels of creatinine — the waste that kidneys filter out of blood. But the race of a patient can only be bucketed into two groups: Black, or not Black. That’s based on a flawed assumption that dates back to the formula’s creation, when medical experts presumed that Black people have higher muscle mass on average, leading to higher kidney function.
Push to remove racist bias from kidney testing gains new ground
For years, physicians and medical students, many of them Black, have warned that the most widely used kidney test — the results of which are based on race — is racist and dangerously inaccurate. Their appeals are gaining new traction, with a wave of petitions and papers calling renewed attention to the issue.
In recent weeks, physicians and medical students at a handful of prominent universities have called on their administrations to end the use of race-based kidney testing, pointing to such changes at Beth Israel Deaconess Medical Center in 2017 and at Mass General Brigham and the University of Washington earlier this summer.
On the heels of those petitions, as well as a widely circulated New England Journal of Medicine analysis of the kidney test and other medical tools that are biased against Black patients, the National Kidney Foundation and the American Society of Nephrology announced this month that they will convene a task force to evaluate the use of race in kidney testing. https://www.nejm.org/doi/full/10.1056/NEJMms2004740
“[Science] has been a conspirator of racism since the genesis of racism. And it is our duty as physicians to be keenly aware and critical of that history, and how we still operate within it despite our best intentions,” said Paloma Orozco Scott, a medical student who co-authored a petition to Mount Sinai calling to end the use of race as a factor in the test.
The test — which measures what’s known as estimated glomerular filtration rate, or eGFR — has historically considered four factors: age, gender, race, and levels of creatinine — the waste that kidneys filter out of blood. But the race of a patient can only be bucketed into two groups: Black, or not Black. That’s based on a flawed assumption that dates back to the formula’s creation, when medical experts presumed that Black people have higher muscle mass on average, leading to higher kidney function.
[OA] Myositis, Rhabdomyolysis and Severe Hypercalcaemia In A Body Builder
Summary: A 53-year-old man who used growth hormone (GH), anabolic steroids and testosterone (T) for over 20 years presented with severe constipation and hypercalcaemia. He had benign prostatic hyperplasia and renal stones but no significant family history. Investigations showed –
(1) corrected calcium (reference range) 3.66 mmol/L (2.2-2.6), phosphate 1.39 mmol/L (0.80-1.50), and PTH 2 pmol/L (1.6-7.2);
(2) urea 21.9 mmol/L (2.5-7.8), creatinine 319 mmol/L (58-110), eGFR 18 mL/min (>90), and urine analysis (protein 4+, glucose 4+, red cells 2+);
(3) creatine kinase 7952 U/L (40-320), positive anti Jo-1, and Ro-52 antibodies;
(4) vitamin D 46 nmol/L (30-50), vitamin D3 29 pmol/L (55-139), vitamin A 4.65 mmol/L (1.10-2.60), and normal protein electrophoresis;
(5) normal CT thorax, abdomen and pelvis and MRI of muscles showed 'inflammation', myositis and calcification;
(6) biopsy of thigh muscles showed active myositis, chronic myopathic changes and mineral deposition and of the kidneys showed positive CD3 and CD45, focal segmental glomerulosclerosis and hypercalcaemic tubular changes; and
(7) echocardiography showed left ventricular hypertrophy (likely medications and myositis contributing), aortic stenosis and an ejection fraction of 44%, and MRI confirmed these with possible right coronary artery disease.
Hypercalcaemia was possibly multifactorial –
(1) calcium release following myositis, rhabdomyolysis and acute kidney injury;
(2) possible primary hyperparathyroidism (a low but detectable PTH); and
(3) hypervitaminosis A.
He was hydrated and given pamidronate, mycophenolate and prednisolone. Following initial biochemical and clinical improvement, he had multiple subsequent admissions for hypercalcaemia and renal deterioration. He continued taking GH and T despite counselling but died suddenly of a myocardial infarction.
Learning points: The differential diagnosis of hypercalcaemia is sometimes a challenge. Diagnosis may require multidisciplinary expertise and multiple and invasive investigations. There may be several disparate causes for hypercalcaemia, although one usually predominates. Maintaining 'body image' even with the use of harmful drugs may be an overpowering emotion despite counselling about their dangers.
Ravindran R, Witczak J, Bahl S, Premawardhana LDKE, Adlan M. Myositis, rhabdomyolysis and severe hypercalcaemia in a body builder [published online ahead of print, 2020 Jul 5]. Endocrinol Diabetes Metab Case Rep. 2020;2020:20-0032. doi:10.1530/EDM-20-0032 Myositis, rhabdomyolysis and severe hypercalcaemia in a body builder in: Endocrinology, Diabetes & Metabolism Case Reports Volume 2020 Issue 1 (2020)
Summary: A 53-year-old man who used growth hormone (GH), anabolic steroids and testosterone (T) for over 20 years presented with severe constipation and hypercalcaemia. He had benign prostatic hyperplasia and renal stones but no significant family history. Investigations showed –
(1) corrected calcium (reference range) 3.66 mmol/L (2.2-2.6), phosphate 1.39 mmol/L (0.80-1.50), and PTH 2 pmol/L (1.6-7.2);
(2) urea 21.9 mmol/L (2.5-7.8), creatinine 319 mmol/L (58-110), eGFR 18 mL/min (>90), and urine analysis (protein 4+, glucose 4+, red cells 2+);
(3) creatine kinase 7952 U/L (40-320), positive anti Jo-1, and Ro-52 antibodies;
(4) vitamin D 46 nmol/L (30-50), vitamin D3 29 pmol/L (55-139), vitamin A 4.65 mmol/L (1.10-2.60), and normal protein electrophoresis;
(5) normal CT thorax, abdomen and pelvis and MRI of muscles showed 'inflammation', myositis and calcification;
(6) biopsy of thigh muscles showed active myositis, chronic myopathic changes and mineral deposition and of the kidneys showed positive CD3 and CD45, focal segmental glomerulosclerosis and hypercalcaemic tubular changes; and
(7) echocardiography showed left ventricular hypertrophy (likely medications and myositis contributing), aortic stenosis and an ejection fraction of 44%, and MRI confirmed these with possible right coronary artery disease.
Hypercalcaemia was possibly multifactorial –
(1) calcium release following myositis, rhabdomyolysis and acute kidney injury;
(2) possible primary hyperparathyroidism (a low but detectable PTH); and
(3) hypervitaminosis A.
He was hydrated and given pamidronate, mycophenolate and prednisolone. Following initial biochemical and clinical improvement, he had multiple subsequent admissions for hypercalcaemia and renal deterioration. He continued taking GH and T despite counselling but died suddenly of a myocardial infarction.
Learning points: The differential diagnosis of hypercalcaemia is sometimes a challenge. Diagnosis may require multidisciplinary expertise and multiple and invasive investigations. There may be several disparate causes for hypercalcaemia, although one usually predominates. Maintaining 'body image' even with the use of harmful drugs may be an overpowering emotion despite counselling about their dangers.
Ravindran R, Witczak J, Bahl S, Premawardhana LDKE, Adlan M. Myositis, rhabdomyolysis and severe hypercalcaemia in a body builder [published online ahead of print, 2020 Jul 5]. Endocrinol Diabetes Metab Case Rep. 2020;2020:20-0032. doi:10.1530/EDM-20-0032 Myositis, rhabdomyolysis and severe hypercalcaemia in a body builder in: Endocrinology, Diabetes & Metabolism Case Reports Volume 2020 Issue 1 (2020)
[OA] Testosterone Replacement Therapy (TRT) is Associated with Delayed Progression of Chronic Kidney Disease
Background - Testosterone replacement therapy (TRT) is used to treat patients with ESRD, but its effects at earlier stages of CKD are unknown.
Study design - Population based retrospective cohort observational study.
Setting and participants - Eligible subjects from Veterans Administration Informatics and Computing Infrastructure (VINCI) were included in the study and divided into two groups namely, (1) Treated to normalize Total Testosterone (TT) and, (2) Untreated.
Predictor - Increase in serum creatinine (mg/dl) over time was taken as a measure of progression of CKD during follow up (FU) years. Data were analyzed using SPSS and SAS. Individual inversed weight probability matching was used to adjust groups. Results were compared using Kaplan Meier survival curves, hazard ratios (HR) and t-test.
Results - Group 1 normalized TT following TRT (N = 38706, creatinine 1.06 ± 0.001, FU 6.1 years) and those in Group 2 maintained low T levels (N = 9755, creatinine 1.11 ± 0.004, FU 5.1 years). Group 1 showed significant increase in days to reach creatinine to > 1.5, (p < 0.0001) and > 3.0 mg/dl (p < 0.0247) indicating delayed progression of CKD. ESRD (creatinine > 6.0 mg/dl) was delayed by 284 days (HR 0.734, p < 0.05 vs. Group 2). TRT was associated with increase in life span by 328 days (HR 0.753, p < 0.0005 vs. group 2) indicating that TRT delayed death.
Limitations - Observational studies may induce unmeasured confounding or hidden bias. There was no randomization due to unavailability of complete clinical data indicating TRT. Thus, the possibility of selection bias cannot be ruled out.
Conclusion - TRT is not associated with significant adverse outcomes in early stages of CKD but rather, with a significant decrease and delay in all-cause mortality, and with delay in progression to ESRD.
Sharma R, Oni O, Wiegmann P, et al. (2020) Testosterone Replacement Therapy (TRT) is Associated with Delayed Progression of Chronic Kidney Disease: A Retrospective Analysis of Testosterone Normalization in US Veterans. Ann Nephrol 5(1):51-59. Testosterone Replacement Therapy (TRT) is Associated with Delayed Progression of Chronic Kidney Disease: A Retrospective Analysis of Testosterone Normalization in US Veterans
Background - Testosterone replacement therapy (TRT) is used to treat patients with ESRD, but its effects at earlier stages of CKD are unknown.
Study design - Population based retrospective cohort observational study.
Setting and participants - Eligible subjects from Veterans Administration Informatics and Computing Infrastructure (VINCI) were included in the study and divided into two groups namely, (1) Treated to normalize Total Testosterone (TT) and, (2) Untreated.
Predictor - Increase in serum creatinine (mg/dl) over time was taken as a measure of progression of CKD during follow up (FU) years. Data were analyzed using SPSS and SAS. Individual inversed weight probability matching was used to adjust groups. Results were compared using Kaplan Meier survival curves, hazard ratios (HR) and t-test.
Results - Group 1 normalized TT following TRT (N = 38706, creatinine 1.06 ± 0.001, FU 6.1 years) and those in Group 2 maintained low T levels (N = 9755, creatinine 1.11 ± 0.004, FU 5.1 years). Group 1 showed significant increase in days to reach creatinine to > 1.5, (p < 0.0001) and > 3.0 mg/dl (p < 0.0247) indicating delayed progression of CKD. ESRD (creatinine > 6.0 mg/dl) was delayed by 284 days (HR 0.734, p < 0.05 vs. Group 2). TRT was associated with increase in life span by 328 days (HR 0.753, p < 0.0005 vs. group 2) indicating that TRT delayed death.
Limitations - Observational studies may induce unmeasured confounding or hidden bias. There was no randomization due to unavailability of complete clinical data indicating TRT. Thus, the possibility of selection bias cannot be ruled out.
Conclusion - TRT is not associated with significant adverse outcomes in early stages of CKD but rather, with a significant decrease and delay in all-cause mortality, and with delay in progression to ESRD.
Sharma R, Oni O, Wiegmann P, et al. (2020) Testosterone Replacement Therapy (TRT) is Associated with Delayed Progression of Chronic Kidney Disease: A Retrospective Analysis of Testosterone Normalization in US Veterans. Ann Nephrol 5(1):51-59. Testosterone Replacement Therapy (TRT) is Associated with Delayed Progression of Chronic Kidney Disease: A Retrospective Analysis of Testosterone Normalization in US Veterans
[OA] miRNAs as Novel Biomarkers of Chronic Kidney Injury in Anabolic-Androgenic Steroid Users
miRNAs are a family of 20-22 non-coding nucleotides that control gene expression by inhibiting the translation of their target messenger RNAs (mRNAs). Two models have been proposed to elucidate the mechanism of action:
· they act either hindering mRNA translation or
· enhancing mRNA degradation.
Anabolic-Androgenic Steroids (AASs) represent a class of drugs used to treat several diseases. In the last few years, AASs have frequently been used for aesthetic purposes, indeed, they form part of the larger group called image- and performance-enhancing drugs (IPEDs).
Long-term AAS use can lead to serious health consequences. In this regard, the present study aimed to analyze the role of several microRNAs (miRNAs) in renal damage after AAS use, to better understand the underlying mechanisms.
For this purpose, two miRNAs (miR-21 and miR-205) were tested in two groups:
· AAS group (seven males, mean age 33.28 ± 4.68 years; mean body mass index (BMI) 27.04 ± 1.07), and
· chronic kidney disease (CKD) group (seven males, mean age 66.2 ± 5.4 years; mean BMI 24.75 ± 1.35).
Finally, the same miRNAs were tested in the "Control" group (seven males, mean age 44.85 ± 5.75 years; mean BMI 26.5 ± 1.88). Kolmogorov-Smirnov Test was used to determine the normality of data distribution. All variables were normally distributed. Student's t-test was used for comparisons between two groups.
Analyzing the results of the present study, the two tested miRNAs (miR-21 and miR-205) were significantly higher in the CKD group compared to the AAS group, with mir-21 being much more expressed than miR-205.
This study represents a pilot study to define if these expression patterns could be studied in other biological samples (plasma, urine) in subjects with different kidney injury linked to chronic kidney diseases and AAS use, to identify reliable biomarkers that could be applied in clinical and forensic diagnostics, as well as a target for toxicological investigations or therapeutic treatments.
Sessa F, Salerno M, Bertozzi G, Cipolloni L, Messina G, Aromatario M, Polo L, Turillazzi E, Pomara C. miRNAs as Novel Biomarkers of Chronic Kidney Injury in Anabolic-Androgenic Steroid Users: An Experimental Study. Front Pharmacol. 2020 Sep 16;11:563756. doi: 10.3389/fphar.2020.563756. PMID: 33041804; PMCID: PMC7525215. miRNAs as Novel Biomarkers of Chronic Kidney Injury in Anabolic-Androgenic Steroid Users: An Experimental Study
miRNAs are a family of 20-22 non-coding nucleotides that control gene expression by inhibiting the translation of their target messenger RNAs (mRNAs). Two models have been proposed to elucidate the mechanism of action:
· they act either hindering mRNA translation or
· enhancing mRNA degradation.
Anabolic-Androgenic Steroids (AASs) represent a class of drugs used to treat several diseases. In the last few years, AASs have frequently been used for aesthetic purposes, indeed, they form part of the larger group called image- and performance-enhancing drugs (IPEDs).
Long-term AAS use can lead to serious health consequences. In this regard, the present study aimed to analyze the role of several microRNAs (miRNAs) in renal damage after AAS use, to better understand the underlying mechanisms.
For this purpose, two miRNAs (miR-21 and miR-205) were tested in two groups:
· AAS group (seven males, mean age 33.28 ± 4.68 years; mean body mass index (BMI) 27.04 ± 1.07), and
· chronic kidney disease (CKD) group (seven males, mean age 66.2 ± 5.4 years; mean BMI 24.75 ± 1.35).
Finally, the same miRNAs were tested in the "Control" group (seven males, mean age 44.85 ± 5.75 years; mean BMI 26.5 ± 1.88). Kolmogorov-Smirnov Test was used to determine the normality of data distribution. All variables were normally distributed. Student's t-test was used for comparisons between two groups.
Analyzing the results of the present study, the two tested miRNAs (miR-21 and miR-205) were significantly higher in the CKD group compared to the AAS group, with mir-21 being much more expressed than miR-205.
This study represents a pilot study to define if these expression patterns could be studied in other biological samples (plasma, urine) in subjects with different kidney injury linked to chronic kidney diseases and AAS use, to identify reliable biomarkers that could be applied in clinical and forensic diagnostics, as well as a target for toxicological investigations or therapeutic treatments.
Sessa F, Salerno M, Bertozzi G, Cipolloni L, Messina G, Aromatario M, Polo L, Turillazzi E, Pomara C. miRNAs as Novel Biomarkers of Chronic Kidney Injury in Anabolic-Androgenic Steroid Users: An Experimental Study. Front Pharmacol. 2020 Sep 16;11:563756. doi: 10.3389/fphar.2020.563756. PMID: 33041804; PMCID: PMC7525215. miRNAs as Novel Biomarkers of Chronic Kidney Injury in Anabolic-Androgenic Steroid Users: An Experimental Study
[OA] Advanced Chronic Kidney Disease is a Strong Predictor of Hypogonadism and is Associated with Decreased Lean Tissue Mass
Purpose: In patients with chronic kidney disease (CKD), hypogonadism is more frequent than in the general population and its prevalence ranges between 40% and 60%. The aim of the study was to investigate the prevalence of hypogonadism and its association with kidney function, body composition, inflammatory markers and lipid disorders in patients with CKD.
Materials and Methods: The study population consisted of 112 men aged ≥ 40 years in different stages of CKD: 33 participants with eGFR ≥ 60 mL/min/1.73 m2, 27 men with eGFR 30– 59 mL/min/1.73 m2, 17 predialysis patients with eGFR < 30 mL/min/1.73 m2, and 35 men on hemodialysis therapy three times a week for more than 3 months (G5D stage).
Total testosterone (TT) levels were measured and free testosterone (FT) levels were calculated. Body composition was assessed using bioimpedance spectroscopy (Body Composition Monitor, FMC). Statistical analysis was performed using Statistica version 13.1.
Results: CKD stage was a strong predictor of hypogonadism (providing an information value of 0.83). The weight of evidence technique allowed us to differentiate the high-risk group, which was a group of patients with advanced CKD, defined as eGFR < 30 mL/min/1.73 m2. In this group, the likelihood of hypogonadism was 69.23%.
Another significant predictor of hypogonadism was lean tissue index (LTI). TT and FT levels were significantly lower in the advanced CKD group in comparison to the control group, whereas prolactin, luteinizing hormone and C-reactive protein levels were significantly higher in the advanced CKD group. The LTI was significantly lower in advanced CKD and was positively correlated with TT and FT.
Conclusion: Decreased eGFR and decreased LTI are predictors of hypogonadism associated with CKD. The study results suggest that hypogonadism screening should be carried out when eGFR
Skiba R, Matyjek A, Syryło T, Niemczyk S, Rymarz A. Advanced Chronic Kidney Disease is a Strong Predictor of Hypogonadism and is Associated with Decreased Lean Tissue Mass. Int J Nephrol Renovasc Dis. 2020;13:319-327. [Full text] Advanced Chronic Kidney Disease is a Strong Predictor of Hypogonadism | IJNRD
Purpose: In patients with chronic kidney disease (CKD), hypogonadism is more frequent than in the general population and its prevalence ranges between 40% and 60%. The aim of the study was to investigate the prevalence of hypogonadism and its association with kidney function, body composition, inflammatory markers and lipid disorders in patients with CKD.
Materials and Methods: The study population consisted of 112 men aged ≥ 40 years in different stages of CKD: 33 participants with eGFR ≥ 60 mL/min/1.73 m2, 27 men with eGFR 30– 59 mL/min/1.73 m2, 17 predialysis patients with eGFR < 30 mL/min/1.73 m2, and 35 men on hemodialysis therapy three times a week for more than 3 months (G5D stage).
Total testosterone (TT) levels were measured and free testosterone (FT) levels were calculated. Body composition was assessed using bioimpedance spectroscopy (Body Composition Monitor, FMC). Statistical analysis was performed using Statistica version 13.1.
Results: CKD stage was a strong predictor of hypogonadism (providing an information value of 0.83). The weight of evidence technique allowed us to differentiate the high-risk group, which was a group of patients with advanced CKD, defined as eGFR < 30 mL/min/1.73 m2. In this group, the likelihood of hypogonadism was 69.23%.
Another significant predictor of hypogonadism was lean tissue index (LTI). TT and FT levels were significantly lower in the advanced CKD group in comparison to the control group, whereas prolactin, luteinizing hormone and C-reactive protein levels were significantly higher in the advanced CKD group. The LTI was significantly lower in advanced CKD and was positively correlated with TT and FT.
Conclusion: Decreased eGFR and decreased LTI are predictors of hypogonadism associated with CKD. The study results suggest that hypogonadism screening should be carried out when eGFR
Skiba R, Matyjek A, Syryło T, Niemczyk S, Rymarz A. Advanced Chronic Kidney Disease is a Strong Predictor of Hypogonadism and is Associated with Decreased Lean Tissue Mass. Int J Nephrol Renovasc Dis. 2020;13:319-327. [Full text] Advanced Chronic Kidney Disease is a Strong Predictor of Hypogonadism | IJNRD
The worldwide burden of kidney disease is rising, but public awareness remains limited, underscoring the need for more effective communication by stakeholders in the kidney health community.
Despite this need for clarity, the nomenclature for describing kidney function and disease lacks uniformity. In June 2019, Kidney Disease: Improving Global Outcomes (KDIGO) convened a Consensus Conference with the goal of standardizing and refining the nomenclature used in the English language to describe kidney function and disease, and of developing a glossary that could be used in scientific publications.
Guiding principles of the conference were that the revised nomenclature should be patient-centered, precise, and consistent with nomenclature used in the KDIGO guidelines. Conference attendees reached general consensus on the following recommendations:
(i) to use “kidney“ rather than “renal” or “nephro-” when referring to kidney disease and kidney function;
(ii) to use “kidney failure” with appropriate descriptions of presence or absence of symptoms, signs, and treatment, rather than “end-stage kidney disease”;
(iii) to use the KDIGO definition and classification of acute kidney diseases and disorders (AKD) and acute kidney injury (AKI), rather than alternative descriptions, to define and classify severity of AKD and AKI;
(iv) to use the KDIGO definition and classification of chronic kidney disease (CKD) rather than alternative descriptions to define and classify severity of CKD; and
(v) to use specific kidney measures, such as albuminuria or decreased glomerular filtration rate (GFR), rather than “abnormal” or “reduced” kidney function to describe alterations in kidney structure and function.
A proposed 5-part glossary contains specific items for which there was general agreement. Conference attendees acknowledged limitations of the recommendations and glossary, but they considered standardization of scientific nomenclature to be essential for improving communication.
[OA] Delayed Rhabdomyolysis Secondary To Anabolic-Androgenic Steroid Use
There are literature reports of anabolic-androgenic steroid-induced rhabdomyolysis. Here we describe a case of a patient presenting with acute confusion and rhabdomyolysis, following an unwitnessed seizure. He had a background of alcohol excess. Three days into his admission he developed dysphagia. At first, the patient denied the use of any medication or drugs. However, he later revealed he had used the anabolic steroid 'Anavar' (oxandrolone) for 60 consecutive days ending a month prior to his admission. The brief seizure was itself unlikely to have resulted in the severity of his rhabdomyolysis. Thus, we report a likely case of delayed rhabdomyolysis secondary to anabolic steroid use. The oropharyngeal dysphagia may be secondary to the rhabdomyolysis; there have been cases of this described in literature.
Benjamin A, Anderson A, Zrelec S. Delayed rhabdomyolysis secondary to anabolic-androgenic steroid use. Clin Med (Lond). 2020 Nov;20(6):e260-e261. doi: 10.7861/clinmed.2020-0694. PMID: 33199332. Delayed rhabdomyolysis secondary to anabolic-androgenic steroid use
There are literature reports of anabolic-androgenic steroid-induced rhabdomyolysis. Here we describe a case of a patient presenting with acute confusion and rhabdomyolysis, following an unwitnessed seizure. He had a background of alcohol excess. Three days into his admission he developed dysphagia. At first, the patient denied the use of any medication or drugs. However, he later revealed he had used the anabolic steroid 'Anavar' (oxandrolone) for 60 consecutive days ending a month prior to his admission. The brief seizure was itself unlikely to have resulted in the severity of his rhabdomyolysis. Thus, we report a likely case of delayed rhabdomyolysis secondary to anabolic steroid use. The oropharyngeal dysphagia may be secondary to the rhabdomyolysis; there have been cases of this described in literature.
Benjamin A, Anderson A, Zrelec S. Delayed rhabdomyolysis secondary to anabolic-androgenic steroid use. Clin Med (Lond). 2020 Nov;20(6):e260-e261. doi: 10.7861/clinmed.2020-0694. PMID: 33199332. Delayed rhabdomyolysis secondary to anabolic-androgenic steroid use
[OA] Abolish Race Correction
Several years ago my daughter sent me an alarming text. She copied the results of her routine blood work and wrote, “Look at eGFR!”. Under the estimated glomerular filtration rate (eGFR) were listed two numbers—one for non-African Americans and a higher one for African Americans. I was floored.
Did this automatic adjustment mean the doctor interpreted my daughter's eGFR differently based simply on her racial identity?
The test's categories themselves made no biological sense. “African American”, like all racialised populations, is a socially constructed grouping. In the USA, individuals with any amount of discernible African ancestry fit the definition—irrespective of the rest of their ancestral backgrounds.
Although my daughter and I identify solely as Black, my mother was a Black Jamaican and my father was the son of white Welsh and German immigrants to the USA. The eGFR disregarded the fabricated nature of the racial distinction it made in calculating kidney function.
I later learned that eGFR race “correction” stems from study findings that participants who self-reported as Black, on average, released more creatinine than white participants for a given kidney function, which historically was attributed to Black people's assumed higher muscle mass.
Recent studies have challenged the muscle-mass hypothesis, but the upward adjustment for all Black patients remains embedded in eGFR calculations. Whatever the flawed rationale, there must be a better way to measure kidney function accurately than by using race—a social classification whose delineations change across time, geography, and political priorities.
Yet misguided ideas about race continue to feature in medicine. I was also dismayed when data on COVID-19 cases and deaths revealed staggering—and strikingly similar—racial disparities in the USA and the UK. As of Dec 10, 2020, the age-adjusted US mortality rates for COVID-19 for Black, Latinx, and Indigenous people were more than 2·7 times higher than for white people.
The greater COVID-19 burden on these populations is not surprising: it stems from structural racism that impaired their health before the pandemic—eg, disproportionate exposure to unhealthy food, environmental toxins, shoddy housing, inadequate health care, and stress from racial discrimination—and forced them into risky front-line jobs with greater exposure to infection. Yet some researchers speculated that these unequal outcomes might be caused by Black people's innate susceptibility—potentially resuscitating the same false racial concepts that underlie race correction.
Roberts DE. Abolish race correction. The Lancet 2021;397:17-8. Redirecting
Several years ago my daughter sent me an alarming text. She copied the results of her routine blood work and wrote, “Look at eGFR!”. Under the estimated glomerular filtration rate (eGFR) were listed two numbers—one for non-African Americans and a higher one for African Americans. I was floored.
Did this automatic adjustment mean the doctor interpreted my daughter's eGFR differently based simply on her racial identity?
The test's categories themselves made no biological sense. “African American”, like all racialised populations, is a socially constructed grouping. In the USA, individuals with any amount of discernible African ancestry fit the definition—irrespective of the rest of their ancestral backgrounds.
Although my daughter and I identify solely as Black, my mother was a Black Jamaican and my father was the son of white Welsh and German immigrants to the USA. The eGFR disregarded the fabricated nature of the racial distinction it made in calculating kidney function.
I later learned that eGFR race “correction” stems from study findings that participants who self-reported as Black, on average, released more creatinine than white participants for a given kidney function, which historically was attributed to Black people's assumed higher muscle mass.
Recent studies have challenged the muscle-mass hypothesis, but the upward adjustment for all Black patients remains embedded in eGFR calculations. Whatever the flawed rationale, there must be a better way to measure kidney function accurately than by using race—a social classification whose delineations change across time, geography, and political priorities.
Yet misguided ideas about race continue to feature in medicine. I was also dismayed when data on COVID-19 cases and deaths revealed staggering—and strikingly similar—racial disparities in the USA and the UK. As of Dec 10, 2020, the age-adjusted US mortality rates for COVID-19 for Black, Latinx, and Indigenous people were more than 2·7 times higher than for white people.
The greater COVID-19 burden on these populations is not surprising: it stems from structural racism that impaired their health before the pandemic—eg, disproportionate exposure to unhealthy food, environmental toxins, shoddy housing, inadequate health care, and stress from racial discrimination—and forced them into risky front-line jobs with greater exposure to infection. Yet some researchers speculated that these unequal outcomes might be caused by Black people's innate susceptibility—potentially resuscitating the same false racial concepts that underlie race correction.
Roberts DE. Abolish race correction. The Lancet 2021;397:17-8. Redirecting
malfeasance
Well-known Member
Is the eGFR different because of racism or because African heritage results in a higher range of "normal?" This question ought to be able to be answered scientifically without all the anguish about racism.
Causal Effects of Relative Fat, Protein, and Carbohydrate Intake on Chronic Kidney Disease
Background - The effects of specific macronutrients on kidney function independent of total calorie intake have rarely been studied, although the composition of macronutrient intake has been reported to affect health outcomes.
Objectives - We aimed to investigate the effects of macronutrient intake ratios on the risk of chronic kidney disease (CKD) by Mendelian randomization (MR) analysis.
Methods - The study was an observational cohort study mainly based on the UK Biobank and including MR analysis. First, we evaluated the relative baseline macronutrient composition—that is, the number of calories from each macronutrient divided by total calorie intake—of the diets of UK Biobank participants, and we used Cox regression to assess the incidence of end-stage kidney disease (ESKD) in 65,164 participants with normal kidney function [estimated glomerular filtration rate (eGFR) ≥60 mL/min/1.73 m2].
We implemented a genetic instrument for relative fat, protein, and carbohydrate intake developed by a previous genome-wide association study (GWAS) and performed MR analysis. Two-sample MR was performed with the summary statistics from independent CKDGen GWAS for kidney function traits (n = 567,460), including CKD (eGFR <60 mL/min/1.73 m2) and log-transformed eGFR.
Results - The median relative macronutrient intake composition at baseline was 35% fats, 15% protein, and 50% carbohydrates. Higher relative protein intake in subjects with normal kidney function was significantly associated with a lower risk of incident ESKD (HR: 0.54; 95% CI: 0.30, 0.95) in the observational investigation.
Two-sample MR indicated that increased relative fat intake causally increased the risk of kidney function impairment [CKD (OR: 1.94; 95% CI: 1.39, 2.71); log eGFR (β: −0.036; 95% CI: −0.048, −0.024)] and that higher relative protein intake was causally linked to a lower CKD risk [CKD (OR: 0.50; 95% CI: 0.35, 0.72); log eGFR (β: 0.044; 95% CI: 0.030, 0.058)].
Conclusions - A desirable macronutrient composition, including high relative protein intake and low relative fat intake, may causally reduce the risk of CKD in the general population.
Park S, Lee S, Kim Y, et al. Causal effects of relative fat, protein, and carbohydrate intake on chronic kidney disease: a Mendelian randomization study. The American Journal of Clinical Nutrition 2021. Causal effects of relative fat, protein, and carbohydrate intake on chronic kidney disease: a Mendelian randomization study
Background - The effects of specific macronutrients on kidney function independent of total calorie intake have rarely been studied, although the composition of macronutrient intake has been reported to affect health outcomes.
Objectives - We aimed to investigate the effects of macronutrient intake ratios on the risk of chronic kidney disease (CKD) by Mendelian randomization (MR) analysis.
Methods - The study was an observational cohort study mainly based on the UK Biobank and including MR analysis. First, we evaluated the relative baseline macronutrient composition—that is, the number of calories from each macronutrient divided by total calorie intake—of the diets of UK Biobank participants, and we used Cox regression to assess the incidence of end-stage kidney disease (ESKD) in 65,164 participants with normal kidney function [estimated glomerular filtration rate (eGFR) ≥60 mL/min/1.73 m2].
We implemented a genetic instrument for relative fat, protein, and carbohydrate intake developed by a previous genome-wide association study (GWAS) and performed MR analysis. Two-sample MR was performed with the summary statistics from independent CKDGen GWAS for kidney function traits (n = 567,460), including CKD (eGFR <60 mL/min/1.73 m2) and log-transformed eGFR.
Results - The median relative macronutrient intake composition at baseline was 35% fats, 15% protein, and 50% carbohydrates. Higher relative protein intake in subjects with normal kidney function was significantly associated with a lower risk of incident ESKD (HR: 0.54; 95% CI: 0.30, 0.95) in the observational investigation.
Two-sample MR indicated that increased relative fat intake causally increased the risk of kidney function impairment [CKD (OR: 1.94; 95% CI: 1.39, 2.71); log eGFR (β: −0.036; 95% CI: −0.048, −0.024)] and that higher relative protein intake was causally linked to a lower CKD risk [CKD (OR: 0.50; 95% CI: 0.35, 0.72); log eGFR (β: 0.044; 95% CI: 0.030, 0.058)].
Conclusions - A desirable macronutrient composition, including high relative protein intake and low relative fat intake, may causally reduce the risk of CKD in the general population.
Park S, Lee S, Kim Y, et al. Causal effects of relative fat, protein, and carbohydrate intake on chronic kidney disease: a Mendelian randomization study. The American Journal of Clinical Nutrition 2021. Causal effects of relative fat, protein, and carbohydrate intake on chronic kidney disease: a Mendelian randomization study
malfeasance
Well-known Member
Whoa! Higher protein intake was significantly associated with a lower risk of end stage kidney disease and chronic kidney disease? That is the opposite of what most believe.
Fat intake was the opposite - and I had never thought about fat intake and kidneys.
Fat intake was the opposite - and I had never thought about fat intake and kidneys.
This is shocking. I thought people with CKD needed lower protein and carb diets. Like keto
A few years ago I had an issue where my GFR dropped to 77. Couldn't understand why. I was on TRT and would blast and cruise. I was sent to a nephrologist and the minute he saw me, he emphatically told me, no way do you have kidney disease. I was already on 40mg a day of lisinopril and blood pressure was 110/60 pretty much all of the time. Even when I would run harsh compounds like tren etc. Most of the damage or diseases that is ever done to kidneys comes from genetics, acute injuries, diabetes, other diseases such as lupus and the biggest one of all high blood pressure.
My creatinine level will always be elevated on lisinopril because it basically widens the renal artery to relieve stress from high blood pressure and in return things like potassium and creatinine stay in the blood longer because they aren't forcefully pushed out.
I asked about certain metabolites like that from Tren and he told me from the research that is out there, there isn't anything in concrete that says the metabolites are damaging. However he did say oral steroids that beat up the liver can sometimes manifest itself down to the kidneys as well too.
Also the way that kidney disease is diagnosed is a joke. Most nephrologist these days use a body mass calculation to figure out true GFR and even then, that not accurate. I had ultrasounds done on my kidneys and they showed no scarring and were normal in size....and trust me, I did a lot of dumb shit. I way more reserved now. That's why it's important to make sure that if your on AAS, you are donating blood regularly, staying hydrated and getting bloods done hopefully twice a year.
My creatinine level will always be elevated on lisinopril because it basically widens the renal artery to relieve stress from high blood pressure and in return things like potassium and creatinine stay in the blood longer because they aren't forcefully pushed out.
I asked about certain metabolites like that from Tren and he told me from the research that is out there, there isn't anything in concrete that says the metabolites are damaging. However he did say oral steroids that beat up the liver can sometimes manifest itself down to the kidneys as well too.
Also the way that kidney disease is diagnosed is a joke. Most nephrologist these days use a body mass calculation to figure out true GFR and even then, that not accurate. I had ultrasounds done on my kidneys and they showed no scarring and were normal in size....and trust me, I did a lot of dumb shit. I way more reserved now. That's why it's important to make sure that if your on AAS, you are donating blood regularly, staying hydrated and getting bloods done hopefully twice a year.
Resurrecting an old but important thread.
Resurrecting an old but very important thread. I've been doing this since 1972 and started to hear and learn about steroids in the 80s. I was living in Cali at the time and trained at Golds, where all of us, including the pros, went to Dr. Walczak. It was always the liver that was the concern. No one thought or talked about the kidneys. Now, as the limits are being pushed, it seems that it is the kidney function that is also being compromised and of much more concern simply because, unlike the liver, the kidneys don't come back.
Can Dr. Scally, or anyone else, interpret his post? I'm not sure how many here are familiar and educated enough to make sense of statements like:
"results revealed a significant increase in the nephrin and podocin gene expression, plasma cystatin C, and the amount of 8-OHdG in the kidney tissue;"
Is that good or bad? What about:
"nandrolone with strenuous exercise groups, showed histological changes such as fibrosis and kidney tissue cells proliferation."
Kidney cell proliferation sounds like a good thing to me. Like it's regenerating.
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