Metabolic Nephropathy - Dr. Gawad
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This document discusses metabolic nephropathy and includes the following key points: 1. It outlines topics on metabolic syndrome, hyperuricemia, nephrolithiasis, and other inborn errors of metabolism. 2. There is conflicting evidence on whether to treat asymptomatic hyperuricemia in chronic kidney disease patients not on dialysis. While guidelines suggest not treating, some special cases may warrant treatment. 3. Evaluating for inborn errors of metabolism is important for understanding nephrolithiasis, as these errors can cause tubular and glomerular kidney disorders.
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Metabolic Nephropathy - Dr. Gawad
- 1. Metabolic Nephropathy Mohammed Abdel Gawad Nephrology Consultant - Alexandria MD Nephrology - Mansoura University drgawad@gmail.com
- 2. To download the lecture with full animations contact me drgawad@gmail.com For more Nephrology lectures visit www.NephroTube.com
- 3. Talk Outline • Metabolic syndrome • Hyperuricemia • Nephrolithiasis • Other inborn errors of metabolism
- 4. Talk Outline • Metabolic syndrome • Hyperuricemia • Nephrolithiasis • Other inborn errors of metabolism
- 5. Published online 2019 Apr 3
- 6. Transl Res. 2017 May; 183: 14–25
- 7. November 2013, 24 (11) 1727-1736
- 11. 2017;67:54‐61
- 12. Sep, 2019; 72(3): 276–279
- 17. Nat Rev Nephrol. 2017 Jan;13(1):11-26 SGLT2-i
- 18. Terminated early 2019 Jun 13;380(24):2295-2306 The risk was lower in the canagliflozin group than in the placebo group: • doubling of serum creatinine • sustained eGFR of <15 ml/min • time to dialysis or kidney transplantation • renal or CV mortality
- 20. https://www.escardio.org/The-ESC/Press-Office/Press-releases/DAPA Abstract title: Dapagliflozin And Prevention of Adverse outcomes in Chronic Kidney Disease.
- 21. Talk Outline • Metabolic syndrome • Hyperuricemia • Nephrolithiasis • Other inborn errors of metabolism
- 22. Talk Outline • Metabolic syndrome • Hyperuricemia • Nephrolithiasis • Other inborn errors of metabolism
- 25. Chronic symptomatic hyperuricemia / Gout / Nephrolithiasis CKD ND Treat hyperuricemia: life style + urate lowering therapy (ULT) CKD Chronic symptomatic hyperuricemia Treat hyperuricemia: life style + urate lowering therapy (ULT) Chronic symptomatic hyperuricemia Asymptomatic hyperuricemia ?? CKD
- 26. Chronic symptomatic hyperuricemia / Gout / Nephrolithiasis CKD ND Treat hyperuricemia: life style + urate lowering therapy (ULT) CKD Chronic symptomatic hyperuricemia / Gout / Nephrolithiasis Treat hyperuricemia: life style + urate lowering therapy (ULT) Chronic symptomatic hyperuricemia Asymptomatic hyperuricemia ?? CKD ND
- 27. Chronic symptomatic hyperuricemia / Gout / Nephrolithiasis CKD ND Treat hyperuricemia: life style + urate lowering therapy (ULT) CKD Chronic symptomatic hyperuricemia / Gout / Nephrolithiasis Treat hyperuricemia: life style + urate lowering therapy (ULT) Chronic symptomatic hyperuricemia Asymptomatic hyperuricemia ?? CKD ND
- 28. Chronic symptomatic hyperuricemia / Gout / Nephrolithiasis CKD ND Treat hyperuricemia: life style + urate lowering therapy (ULT) CKD Chronic symptomatic hyperuricemia / Gout / Nephrolithiasis Treat hyperuricemia: life style + urate lowering therapy (ULT) Chronic symptomatic hyperuricemia Asymptomatic hyperuricemia ?? ULT: to use or not to use CKD ND life style
- 29. Chronic symptomatic hyperuricemia / Gout / Nephrolithiasis CKD ND Treat hyperuricemia: life style + urate lowering therapy (ULT) CKD Chronic symptomatic hyperuricemia / Gout / Nephrolithiasis Treat hyperuricemia: life style + urate lowering therapy (ULT) Chronic symptomatic hyperuricemia Asymptomatic hyperuricemia ?? ULT: to use or not to use CKD ND life style
- 30. Chronic symptomatic hyperuricemia Asymptomatic hyperuricemia ?? ULT: to use or not to use CKD ND • Available evidence and its appraisal: • Guidelines • Trials / Studies • Special situations • Proposed approach
- 31. Chronic symptomatic hyperuricemia Asymptomatic hyperuricemia ?? ULT: to use or not to use CKD ND • Available evidence and its appraisal: • Guidelines • Trials / Studies • Special situations • Proposed approach Conflicting and contradictory results
- 32. Chronic symptomatic hyperuricemia Asymptomatic hyperuricemia ?? ULT: to use or not to use CKD ND • Available evidence and its appraisal: • Guidelines • Trials / Studies • Special situations • Proposed approach Conflicting and contradictory results
- 35. Available online 15 May 2020
- 37. Chronic symptomatic hyperuricemia Asymptomatic hyperuricemia ?? ULT: to use or not to use CKD ND • Available evidence and its appraisal: • Guidelines • Trials / Studies • Special situations • Proposed approach Conflicting and contradictory results
- 43. no evidence of clinically meaningful benefits of serum urate reduction with allopurinol on kidney outcomes among patients with type 1 diabetes and early-to-moderate diabetic kidney disease
- 44. no evidence of clinically meaningful benefits of serum urate reduction with allopurinol on kidney outcomes among patients with type 1 diabetes and early-to-moderate diabetic kidney disease Can PERL study result be generalized to all type 1 DM CKD patients?
- 49. Can CKD-FIX study result be generalized to all CKD with albuminuric or high risk of progression?
- 51. stage 3 or 4 CKD
- 52. Patients with progressing CKD (decrease in eGFR by >4 ml/min/1.73m2 per year) over 1–2 years, empiric allopurinol may be appropriate
- 53. Patients with progressing CKD (decrease in eGFR by >4 ml/min/1.73m2 per year) over 1–2 years, empiric allopurinol may be appropriate However, several issues were raised in reply to this article, including questions about quality and biases of included studies Vs.
- 55. insufficient power as a result of incomplete enrollment (difficulty recruiting patients who met criteria, possibly indicating limitations in the generalizability of results)
- 57. Chronic symptomatic hyperuricemia Asymptomatic hyperuricemia ?? ULT: to use or not to use CKD ND • Available evidence and its appraisal: • Guidelines • Trials / Studies • Special situations • Proposed approach
- 58. PERL trial and CKD-FIX Young age
- 59. Non proteinuric, mild to moderate renal impairment
- 60. The association between the pre-donation serum UA and residual renal function at 6 months and 1 year after nephrectomy 291 live kidney donors Volume 49, Issue 5, June 2017 Solitary kidney
- 61. Chronic symptomatic hyperuricemia Asymptomatic hyperuricemia ?? ULT: to use or not to use CKD ND • Available evidence and its appraisal: • Guidelines • Trials / Studies • Special situations • Proposed approach
- 62. ?! ?! non proteinuric, mild to moderate CKD, young age, solitary kidney
- 64. Talk Outline • Metabolic syndrome • Hyperuricemia • Nephrolithiasis • Other inborn errors of metabolism
- 65. Talk Outline • Metabolic syndrome • Hyperuricemia • Nephrolithiasis • Other inborn errors of metabolism
- 68. © Springer Nature Switzerland AG 2019
- 69. © Springer Nature Switzerland AG 2019
- 72. Talk Outline • Metabolic syndrome • Hyperuricemia • Nephrolithiasis • Other inborn errors of metabolism
- 73. Talk Outline • Metabolic syndrome • Hyperuricemia • Nephrolithiasis • Other inborn errors of metabolism
- 78. Home Messages • Metabolic syndrome treatment can delay CKD progression • SGLT2-i have reno-protective effects
- 79. Home Messages • Asymptomatic Hyperuricemia in CKD Not on Dialysis: Debatable evidence to treat or not treat Scale arm is more toward not to treat ?! CKD progression (especially after controlling all other factors/early CKD), non proteinuric, mild to moderate CKD, young age, solitary kidney
- 80. Home Messages • Metabolic assessment for nephrolithiasis is important specially in cases with recurrent renal stones. • Errors of metabolism may cause tubular and glomerular renal disorders
Notas del editor
- Renal ultrastructural findings associated with obesity often manifests as focal segmental glomerulosclerosis characterized by glomerulomegaly, podocytopathy, and mesangial expansion presenting with massive proteinuria.
- Due to the complexity of their interrelationships, it is difficult to draw a causal association and discriminate which of the components of MetS gives rise to renal functional deterioration.
- Post hoc, ASN 2019: In patients who had eGFR decreased than 30 = these effects appeared to be consistent among these patients, but the differences between the canagliflozin and placebo groups were not statistically significant. Medscape: It was projected that treatment with canagliflozin can delay progression to end-stage kidney disease by about 15 years in patients aged 30 years or older with T2D (glycated hemoglobin [HbA1c] 6.5% to 12%) and renal insufficiency (eGFR even below 30 mL/min/1.73 m2 with presence of albuminuria) who were on a stable dose of ACE inhibitor or ARB. Based on these data, the FDA approved a new indication for canagliflozin for the treatment of diabetic kidney disease in T2D.
- - Extracellular precipitation in the form of microscopic crystals and macroscopic urate stones can cause structural damage.
- The Voting Panel felt that, on average, for the majority of patients with asymptomatic hyperuricemia (including those with comorbid CKD, CVD, urolithiasis, or hypertension), the benefits of ULT would not outweigh potential treatment costs or risks for the large number of patients unlikely to progress to gout.
- eGFR was determined by the CKD-EPI creatinine equation. Sensitivity analyses were conducted with the use of the CKD-EPI equation, based on cystatin C alone and in combination with creatinine, and the Modification of Diet in Renal Disease equation
- eGFR was determined by the CKD-EPI creatinine equation. Sensitivity analyses were conducted with the use of the CKD-EPI equation, based on cystatin C alone and in combination with creatinine, and the Modification of Diet in Renal Disease equation
- Nevertheless, too many data support the concept that interventions on risk factors may be ineffective once progression of kidney damage is under way and earlier intervention could be advisable in the course of disease.
- Nevertheless, too many data support the concept that interventions on risk factors may be ineffective once progression of kidney damage is under way and earlier intervention could be advisable in the course of disease.
- 30% of patients stopped taking allopurinol, though there was still a sustained mean reduction of serum level of 35% (similar to PERL; 36%)
- Cystinosis, a lysosomal storage disease, is the most common cause [2-5]. However, renal phenotype in these patients may be variable in extent in some cases and may consist a selective proximal tubulopathy rather than real Fanconi syndrome.
- Renal tubular acidosis is characterized by an inability to appropriately acidify the urine along with a normal serum anion gap and it is separated into 3 main types: I (distal), II (proximal) and IV. Type III consists a combined type of proximal and distal renal tubular acidosis