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Chronic Kidney Disease, \, Intrinsic Tubular and Interstitial Disease,…

- - - - nephritic
        
        causes
        
        IgA nephropathy
        
        infective endocarditi
        
        post-streptococcal glomerulosclerosis
        
        lupus nephritis
      - nephrotic
        
        causes
        
        focal segmental glomerulosclerosis
        
        Minimal change disease
        
        membranous glomerulosclerosis
        
        effect
        
        Proteinuria, usually nephrotic range (>3.5 gm per 24 hours), inactive urine microscopy.
    - - causes
        
        fibro-muscular dysplasia
        
        effect Ischemic nephropathy
        
        tubulointerstitial fibrosis
        
        glomerulosclerosis
        
        renal artery stenosis
        
        nephrosclerosis
        
        effect damage to blood vessels, glomeruli, and tubulointerstitium.
    - - Sjogren syndrome,
      - Nephrocalcinosis
      - Polycystic kidney disease
      - effects
        
        Structural and functional abnormalities affecting the tubules and interstitium of the kidneys
  - - - persistently decreased profusion
        
        increase the risk of intrinsic kidney injury
        
        such as tubular necrosis
        
        leads to progressive loss of renal function over time
  - - - obstructive nephropathy
        
        impedes normal urine flow
        
        increased pressure on kindneys
        
        renal parenchymal damage
        
        progressive decline to CKD
- - - - causes hypertension and electrolyte imbalances
  - - - causes bone mineral disorder and cardiovascular complications
  - - - hyperparathyroidism
        
        bone disorders
  - - - causes volume overload and hypertension
- - - - tubules
        
        interstitium
        
        glomeruli
        
        vessels
        
        glomerular filtration rate
        
        G3a: GFR 45 to 59 ml/min per 1.73 m2
        
        G3b: GFR 30 to 44 ml/min per 1.73 m2
        
        G2: GFR 60 to 89 ml/min per 1.73 m2
        
        G4: GFR 15 to 29 ml/min per 1.73 m2
        
        asymptomatic until stages 4 and 5
        
        G1: GFR 90 ml/min per 1.73 m2 and above
        
        G5: GFR less than 15 ml/min per 1.73 m2
      - manifests histologically as
        
        ubulointerstitial fibrosis
        
        vascular sclerosis.
        The sequence of events that lead to scarring an
        
        glomerulosclerosis
        
        Clinical manifestations
        
        Shortness of breath due to pulmonary edema from fluid overload
        
        Hypertension that's difficult to control
        
        Skin pigmentation
        
        Pericardial friction rub due to uremic pericarditis
        
        Uremic frost, where high levels of BUN result in urea in sweat
        
        Nausea
        
        Hypertensive fundal changes suggesting chronicity
        
        Vomiting
        
        Loss of appetite
        
        Fatigue and weakness
        
        Sleep disturbance
        
        Chest pain due to uremic pericarditis
        
        Oliguria
        
        Persistent pruritus
        
        Scratch marks from pruritus
        
        Decreased mental sharpness
        
        Swelling of feet and ankles
        
        Muscle twitches and cramps
        
        Imaging of kidneys
        
        small kidneys
        
        scarring
        
        cysts
        
        reduced cortical thikcness
        
        assessment of proteinuria
        
        albumin-creatinine ratio
        
        1 more item...
        
        assessment of GRE
        
        kidney function tests
        
        electrolyte imbalance
        
        Hyponatremia
        
        Hypercalcemia
        
        Hypocalcemia:
        
        Hyperphosphatemia
        
        Hyperkalemia
        
        Acid-base imbalance
        
        Metabolic acidosis:
        
        Treatments
        
        Medications
        
        1 more item...
        
        Lifestyle changes
        
        7 more items...
        
        dialysis
        
        2 more items...
        
        Supportive treatment
        
        1 more item...
        
        Kindy transplant
  - - - glomerular hypertension
        
        glomerulosclerosis
- - - - CKD-induced electrolyte imbalances and metabolic abnormalities directly affect nerve function, contributing to neuropathy
      - CKD-related vascular alterations impair blood flow to peripheral nerves, worsening nerve damage
      - Toxic metabolites build up due to impaired kidney function, damaging peripheral nerves
  - - - Retained toxins in CKD damage autonomic nerves
        
        CKD-related vascular alterations affect autonomic nerve function, leading to symptoms like postural hypotension and cardiac arrhythmia
        
        CKD frequently accompanies diabetes, a common cause of autonomic neuropathy
  - - - Prevalent in CKD, iron deficiency can worsen RLS symptoms
        
        CKD-related alterations in dopamine metabolism and function may exacerbate RLS symptoms
        
        Retained uremic toxins may disrupt dopaminergic pathways linked to RLS
  - - - CKD-induced electrolyte imbalances can contribute to nerve compression
      - Retained uremic toxins may directly impact nerve function, increasing the likelihood of nerve compression
      - CKD-related edema elevates pressure within the carpal tunnel, compressing the median nerve
  - - - CKD heightens the risk of cerebrovascular issues, like stroke, which impair cognitive function
      - electrolyte imbalances and metabolic abnormalities in CKD disrupt brain function, contributing to cognitive impairment
      - Kidney dysfunction leads to the retention of uremic toxins, impacting brain function
  - - - CKD-related vascular alterations can reduce blood flow to peripheral nerves, increasing the risk of ischemia and neuropathy.
      - Nerve compression by arteriovenous fistulas or grafts for hemodialysis can cause nerve ischemia and damage
  - - - Electrolyte imbalances and metabolic abnormalities in CKD impair muscle function
      - Malnutrition and protein-energy wasting in CKD result in muscle weakness and myopathy.
      - CKD leads to the retention of uremic toxins, directly impacting muscle function and metabolism
- - - - Proinflammatory circulatory mediators progressively increase as kidney function declines
  - - - unregulated glucose
        
        microvascular complications
  - - - Arrhythmias
        
        heart failure
        
        endothelial dysfunction
- - - - CKD activates toll-like receptors, especially TLR-4, by gut-derived bacterial lipopolysaccharides (LPS) from gram-negative bacteria
    - - in CKD, autoimmune kidney diseases can exacerbate gastrointestinal problems through immune-mediated mechanisms.
    - - CKD-associated dysbiosis causes "leaky gut," allowing uremic toxins into the bloodstream, worsening kidney disease and possibly leading to gastrointestinal issues.
    - - CKD-related dysbiosis shifts gut microbiome balance, causing gastrointestinal symptoms like bloating, diarrhea, and constipation
    - - from intestinal metabolism protein in gut bacteria
        
        accumulation disrupts gut microbiome and imbalances gut microbes /dysbiosis
    - - . Diets high in protein and low in fiber may contribute to the production of uremic toxins and dysbiosis,