To prevent chronic renal insufficiency (chronic kidney failure), attention must be paid to reducing individual risk factors. Behavioral risk factors
- Diet
- Consumption of stimulants
- Tobacco (smoking) – favors the progression of renal failure.
- Overweight (BMI ≥ 25; obesity) – HDL levels and glomerular filtration rate decreased with increasing BMI; chronic kidney disease (defined as estimated glomerular filtration rate below 60 ml/min/1.73 m2) was diagnosed 2.6 years later in underweight than in normal weight individuals, whereas it was diagnosed 1.1 years earlier in overweight and 2.0 years earlier in obese individuals
Medications (nephrotoxic – drugs that damage the kidneys/nephrotoxic drugs).
- ACE inhibitors (benazepril, captopril, cilazapril, enalapril, fosinopril, lisinopril, moexipril, peridopril, quinapril, ramipril, spirapril) and AT1 receptor antagonists (candesartan, eprosartan, irbesartan, losartan, olmesartan, valsartan, telmisartan) (acute: Decrease in glomerular filtration rate (GFR) associated with creatinine increase: ACE inhibitors as well as AT1 receptor antagonists abolish vasoconstriction (vasoconstriction) in the vas efferens, and a decrease in GFR and increase in serum creatinine result. Up to 0.1 to 0.3 mg/dl, this is usually tolerable. However, in the presence of hemodynamically relevant renal artery stenosis (not uncommon in patients with atherosclerosis/arteriosclerosis), GFR becomes markedly angiotensin II-dependent impaired, and administration of an ACE inhibitor or AT1 receptor antagonist may result in acute renal failure (ANV))!
- Angiotensin receptor neprilysin antagonists (ARNI) – dual drug combination: sacubitril/valsartan.
- Allopurinol
- Antiphlogistic and antipyretic analgesics (non-steroidal anti-inflammatory drugs (NSAID), non-steroidal anti-inflammatory drugs) or non-steroidal anti-inflammatory drugs (NSAIDs* ) Caution: the combination of a diuretic, an RAS blocker, and an NSAID is associated with a significant risk of acute kidney injury:
- Acetylsalicylic acid (ASA).
- Diclofenac
- Ibuprofen/naproxen
- Indometacin
- Metamizole or novaminsulfone is a pyrazolone derivative and analgesic from the group of non-acidic non-opioid analgesics (highest analgesic and antipyretic activity. Side effects: Circulatory fluctuations, hypersensitivity reactions, and very rarely agranulocytosis.
- Paracetamol / acetaminophen
- Phenacetin (phenacetin nephritis)
- Selective COX-2 inhibitors such as rofecoxib, celecoxib (side effects: decreased sodium and water excretion, blood pressure increase and peripheral edema. This is usually accompanied by hyperkalemia (excess potassium))!
- Antibiotics
- Aminoglycoside antibiotics (aminoglycosides) – amikacin, gentamycin (gentamicin), netilmicin, streptomycin, tobramycin, vancomycin.
- Ampicillin (group of β-lactam antibiotics).
- Cephalosporins (cefotaxime, cefotiam, cefuroxime).
- Amoxicillin
- Carbenicillin
- Ethambutol (tuberculostat)
- Fenoprofen
- Glycopeptide antibiotics (vancomycin) – esp. piperacillin reduces vancomycin clearance.
- Gyrase inhibitors (extremely rare: acute interstitial nephritis after ciprofloaxin, ofloxacin and norfloxacin).
- Methicillin (penicillinase-resistant penicillin).
- Oxacillin
- Rifampicin (bactericidal antibiotic from the group of ansamycins).
- Sulfonamides such as sulfadiazine, cotrimoxazole (fixed combination of: trimethoprim + sulfamethoxazole).
- Tetracyclines (doxycycline)
- Antifungals
- Polyenes (amphotericin B, natamycin)
- Chloral hydrate
- Diuretics
- Thiazide diuretics (hydrochlorothiazide (HCT), benzthiazide, clopamide, chlortalidone (CTDN), chlorothiazide, hydroflumethiazide, indapamide, methyclothiazide, metolazone, polythiazide and trichloromethiazide, xipamide) + elderly patients: Decrease in GFR of more than 25%.
- The combination of a diuretic, an RAS blocker, and an NSAID is associated with a significant risk of acute kidney injury.
- Colchicine
- Diuretics
- D-Penicillamine
- Gold – sodium aurothiomalate, auranofin
- Immunosuppressants (ciclosporin (cyclosporin A)) – esp. ciprofloxacin plus ciclosporin A.
- Interferon
- Colloidal solution with hydroxyl starch
- Contrast media – Of particular importance here are magnetic resonance imaging (MRI) contrast media containing gadolinium, which can lead to nephrogenic systemic fibrosis (NSF). Particularly affected by NSF are patients with a glomerular filtration rate (GFR) of less than 30 ml/min. [CKD stage 4]; iodine-containing radiographic contrast agents; [require prophylactic irrigation in renal insufficiency]EMA (European Medicines Agency): categorization of GBCAs (gadolinium-based contrast agents) in terms of NSF (nephrogenic systemic fibrosis) risk, based on thermodynamic and kinetic properties:High risk:
- Gadoversetamide, gadodiamide (linear/non-ionic chelates) gadopentetate dimeglum (linear/ionic chelate).
Medium risk:
- Gadofosveset, gadoxetic acid disodium, gadobenate dimeglumine (linear/ionic chelates).
Low risk
- Gadoterate meglumine, gadoteridol, gadobutrol (macrocyclic chelates).
If contrast agent is required: observe “renal protection” measures!
- Lithium
- Proton pump inhibitors (PPI; acid blockers).
- “Atherosclerosis Risk in Communities” (ARIC): 10-year PPI use: rate of chronic renal failure in patients on PPI 11.8%, without 8.5%; rate of renal damage: 64%; two pills a day resulted in significantly more frequent damage: 62%
- Geisinger Health System: observation period 6.2 years; rate of chronic renal failure disease: 17%; rate of renal damage: 31%; two pills a day resulted in significantly more frequent damage: 28%
- Rast blockers: the combination of a diuretic, an RAS blocker, and an NSAID is associated with a significant risk of acute kidney injury.
- Tacrolism (macrolide derived from the gram-positive bacterium Streptomyces tsukubaensis. Tacrolimus is used as a drug in the group of immunomodulators or calcineurin inhibitors).
- TNF-α antibodies – adalimumab → IgA nephropathy (the most common form of idiopathic glomerulonephritis in adults, accounting for 30%).
- Antivirals
- Nucleoside analogues (aciclovir, brivudine, cidofovir, famciclovir, foscarnet, ganciclovir, valaciclovir).
- Cytostatic drugs – carboplatin, cisplatin, cyclophosphamide, gemcitabine, iphosphamide (ifosfamide), methotrexate (MTX), mitomycin C, platinum (cisplatin).
Environmental stress – intoxications (poisonings).
- Metals (cadmium, lead, mercury, nickel, chromium, uranium).
- Halogenated hydrocarbons (HFCs; trichloroethene, tetrachloroethene, hexachlorobutadiene, chloroform).
- Herbicides (paraquat, diquat, chlorinated phenoxyacetic acids).
- Mycotoxins (ochratoxin A, citrinin, aflatoxin B1).
- Aliphatic hydrocarbons (2,2,4-trimethylpentane, decalin, unleaded gasoline, mitomycin C).
- Melamine
Prevention factors (protective factors)
- Genetic factors:
- Genetic risk reduction depending on gene polymorphisms:
- Genes/SNPs (single nucleotide polymorphism; English : single nucleotide polymorphism):
- Genes: UMOD
- SNP: rs4293393 in the gene UMOD
- Allele constellation: CT (0.76-fold).
- Allele constellation: CC (0.58-fold)
- Genes/SNPs (single nucleotide polymorphism; English : single nucleotide polymorphism):
- Genetic risk reduction depending on gene polymorphisms:
- Nutrition
- Mediterranean diet: moderate fat and carbohydrate intake led to significantly 30% reduced odds of initial diagnosis of renal failure (odds ratio, OR 0.70); end point “albuminuria” was also significantly less common with healthy diet (OR 0.77):
- Fat intake: monounsaturated fatty acids and omega-3 fatty acids predominated; saturated fatty acids were supplied in very low amounts.
- The following foods are preferably consumed: cereal products, vegetables, salad, legumes, fruits and nuts and fish.
- As low as possible proportions of red meat and meat products (sausages), sodium (table salt) and sweetened beverages.
- Mediterranean diet: moderate fat and carbohydrate intake led to significantly 30% reduced odds of initial diagnosis of renal failure (odds ratio, OR 0.70); end point “albuminuria” was also significantly less common with healthy diet (OR 0.77):
- Reduction of contrast agent-induced nephropathies:
- N-acetylcysteine versus intravenous physiological saline: risk reduction 31%.
- Statins plus N-acetylcysteine versus N-acetylcysteine: risk reduction 48%.