Chronic Kidney Insufficiency: Medical History

Medical history (history of illness) is an important component in the diagnosis of chronic renal failure (chronic kidney disease) or chronic kidney disease. Family history

  • What is the general health status of your relatives?
  • Are there any kidney/urinary tract diseases in your family that are common?

Social history

  • What is your profession?
  • Are you exposed to harmful working substances in your profession?

Current medical history/systemic medical history (somatic and psychological complaints).

  • Do you suffer from hypertension (high blood pressure)?
  • Do you have diabetes mellitus (diabetes)?
  • Have you suffered or are suffering from inflammation of the genitourinary tract (urinary tract organs) or nephritis (inflammation of the kidneys)?
  • Do you suffer from metabolic disorders?
  • Do you notice the following symptoms in yourself:
    • Loss of appetite
    • Nausea/vomiting
    • Dyspnea (shortness of breath)*
    • Edema* (water retention in the tissues).
    • Weight changes
    • Pruritus (itching)
    • Muscle cramps
    • Bone pain
    • Nerve pain
    • Disturbances of consciousness*
  • Do you feel ill?
  • How long have these changes existed?

Vegetative anamnesis including nutritional anamnesis.

  • Has your appetite changed?
  • Has your body weight changed unintentionally?
  • Do you suffer from sleep disorders?
  • Do you smoke? If yes, how many cigarettes, cigars or pipes per day?
  • Do you use drugs? If yes, what drugs and how often per day or per week?

Self history incl. medication history.

  • Pre-existing conditions (cardiovascular disease, diabetes mellitus (diabetes), urological disease).
  • Operations
  • Allergies
  • Environmental pollution
    • 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

Medication history

  • 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 restricted, 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
  • Atypical antipsychotics (olanzapine, quetiapine, risperidone) – elderly patients have approximately 70% increased risk of hospitalization for acute renal failure (ANV) during the first three months of treatment with atypical antipsychotics
  • Antiphlogistic and antipyretic analgesics (non-steroidal anti-inflammatory drugs (NSAID), non-steroidal anti-inflammatory drugs) and non-steroidal anti-inflammatory drugs (NSAID* ), respectively.
    • Adverse effects on renal function especially in the elderly and patients with pre-damaged kidneys or associated risk factors.Younger, physically active adults also have an increased risk of acute and chronic renal damage with frequent NSAID use (> 7 defined daily doses of NSAIDs per month).NSAID-related risk of renal damage was even higher in: BMI ≥ 30, hypertension or diabetes mellitus, or male sex.
    • Note: 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 (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!).
  • Antibiotics
  • Antifungals
  • Chloral hydrate
  • Diuretics
  • Colchicine
  • D-Penicillamine
  • Gold – sodium aurothiomalate, auranofin
  • Hydroxyethyl starch (HES)
  • 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).
  • Lithium
  • Oncological therapy
  • Proton pump inhibitors (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