Therapy goals
- Prevention or slowing of progression (progression) of renal changes (nephroprotection), ie.
- Avoidance of chronic hyperglycemia (hyperglycemia).
- Optimal blood pressure values
- Adjust blood lipids (blood fats) to low levels [primary prevention depending on risk LDL cholesterol levels < 100 mg/dl; if CHD exists, aim for LDL cholesterol < 70 mg/dl (< 1.798 mmo/l)]
- Weight reduction (decrease in proteinuria/increased excretion of protein with urine).
For this purpose, the following parameters must be set optimally:
- HbA1c:
- Primary prevention: 6.5% (48 mmol/mol) to 7.5% (58 mmol/mol); for patients with macroangiopathic complications and/or presence of hypoglycemia unawareness: upper target range (7.0-7.5% [53-58 mmol/mol]
- Secondary prevention: <7.0% (<53 mmol/mol) to prevent progression of diabetic nephropathy.
In moderately to severely impaired renal function, as well as renal replacement therapy (esp. in combination with anemia / anemia), the HbA1c underestimates the quality of metabolic
- Blood pressure (target systolic blood pressure 130-139 mmHg (ESC/ESH guidelines); patients with hypertension and diabetes on target ≤ 130/80 mmHg; patients with diabetes and hypertension who are ≥ 65 years old: Target blood pressure 130-140 mmHg).
Note: The development and progression (progression) of diabetic nephropathy may be accelerated by the following additional factors:
- Increased protein intake
- Smoking
- Anemia (anemia)
- Hyperuricemia (increased uric acid content in the blood).
- Renal acidosis (kidney-related hyperacidity).
Therapy recommendations
- Regarding adequate drug therapy: see Diabetes mellitus type 1/Drug therapy or Diabetes mellitus type 2/Drug therapy.
- ACE inhibitors-in case of intolerance, AT1 blockers-lead to decreased protein excretion (protein excretion) and prevent progression (progression) of the disease (nephroprotection/protection of the kidneys); this occurs by decreasing glomerular filtration pressure and attenuating the profibrogenic and proinflammatory effects of angiotensin II and aldosterone.
- ACE inhibitors-AT1 blockers in case of intolerance-can be combined with calcium antagonists as well as other agents.
- The combination of ACE inhibitors and AT1 blockers and possibly aldosterone antagonists is contraindicated because of the risk of dangerous hyperglycemia (hyperglycemia) (contraindications).
- SGLT2 inhibitors (canagliflozin* ) reduce just in type 2 diabetics with nephropathy the risk of end-stage renal failure (nephroprotection). In a first study, canagliflozin vs. placebo significantly reduced the risk of dialysis, transplantation or sustained GFR < 15 ml/min/1.73 m² by a relative 30 percent.
- ACE inhibitors-in case of intolerance, AT1 blockers-lead to decreased protein excretion (protein excretion) and prevent progression (progression) of the disease (nephroprotection/protection of the kidneys); this occurs by decreasing glomerular filtration pressure and attenuating the profibrogenic and proinflammatory effects of angiotensin II and aldosterone.
- Therapy of dyslipoproteinemia: statins possibly also PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibitors (eg, evolocumab, alirocumab* * ).
- See also under “Further therapy”.
* Per Gesetz zur Neuordnung des Arzneimittelmarkts (AMNOG) taken off the market. * * Per notification of July 18, 2019, withdrawn from the market in Germany for patent reasons. Further notes
- Phase III study: finerenone (nonsteroidal selective mineralocorticoid receptor antagonist (MRA)) delays the progression of diabetic nephropathy (primary endpoint) as well as the risk of cardiovascular events (secondary endpoint) in patients with type 2 diabetes.
Other therapeutic approaches
Furthermore, depending on other risk factors, the following agents should be used:
- Antiplatelet agents (TAH).
- Lipid-lowering agents (drugs used to treat disturbed blood lipid levels).
Tauroursodeoxycholic acid (TUDCA,) which has been used for decades for the treatment and prophylaxis of gallstone disease, can improve the function and survival of human cells. In one study, TUDCA was shown to alleviate the damage of diabetic nephropathy and may partially lead to regeneration of kidney tissue. This demonstrated an additional therapeutic benefit to the current standard therapy, inhibition of the renin-angiotensin-aldosterone system (RAAS inhibition).The authors demonstrated in several experimental models of diabetic nephropathy that combination therapy (RAAS inhibition + TUDCA) was superior to RAAS inhibition alone. Absolutely avoid the use of:
- NSAIDs (nonsteroidal anti-inflammatory drugs).
- X-ray contrast media
- See also chronic renal failure/causes (under nephrotoxic drugs).
