4.3 Renal Diseases Overview

Renal Diseases

• Prevalence: Over 10% of adults aged 20+ in the US have chronic kidney disease, with many experiencing acute kidney injury. Treatable forms exist to slow disease progression.

• Etiology: Common causes include diabetes, hypertension, and autoimmune disorders (like lupus).

• Presentation: Typically asymptomatic until advanced failure, as kidneys lack pain receptors. Pain may occur if the ureter or renal capsule is involved.

• Kidney Function: Kidneys filter blood, metabolize substances, excrete waste, regulate fluid/electrolyte balance, and maintain homeostasis.

Types of Renal Disease

• Categorization: Classified by site of lesion (e.g., tubular interstitial disease), factors leading to the disease (e.g., infectious or toxic glomerular diseases), or clinical presentation (e.g., proteinuria, hematuria).

• Nephrotic Disorders: Often present with immune complex deposition under epithelial cells, affecting foot processes, basement membranes, and potentially causing structural changes.

• Kidney Regions Affected: The glomerulus (initial filter), renal medulla (low oxygen environment), & overall hemodynamics (blood flow) are key areas susceptible to injury.

Acute Kidney Injury (AKI)

• Definition: Rapid deterioration of renal function, characterized by nitrogen waste accumulation (e.g., elevated blood urea nitrogen, serum creatinine), and/or decreased urine output (<0.5 mL/kg/hour for 6+ hours).

• Causes (Pre-renal, Intra-renal, Post-renal): Various, including blood flow issues (hypoperfusion, hypotension), inflammatory diseases, toxic effects (amino glycosides, antibiotics, rhabdomyolysis), and urinary tract obstructions (intrinsic or extrinsic). Sepsis is a prominent cause with both pre and intra renal components.

• Pathophysiology: Deterioration affects filtration, leading to toxin buildup and electrolyte imbalances (sodium, potassium).

• Consequences: Volume/fluid imbalances (edema, hypertension, heart failure), electrolyte/acid-base disturbances, and potential life-threatening complications arise from the build-up of toxins.

Chronic Kidney Disease (CKD)

• Etiology: Primarily caused by diabetes and hypertension, leading to nephron loss and irreversible damage. This causes an elevated burden on remaining nephrons, contributing to further damage.

• Progression: Irreversible loss of nephrons, elevated glomerular filtration rates, hyperfiltration in remaining nephrons, and resulting hypertension, fibrosis, and scarring accelerate nephron destruction.

• Clinical Effects: Waste products (e.g., nitrogen) build-up, hormonal imbalances, fluid/electrolyte imbalances (sodium, potassium, acid/base), cardiovascular complications, bone disorders (calcium, phosphorus), anemia, and impaired blood clotting (hemostasis).

CKD Specific Imbalances

• Sodium & Water: Moderate retention typically occurs without obvious signs but excessive sodium intake worsens fluid retention, contributing to heart failure, hypertension. Restrict sodium intake (≤2 grams/day).

• Potassium (Hyperkalemia): Potentially life-threatening complication, initially compensated through mechanisms that can be impaired by drugs, leading to dangerous imbalances.

• Acid-Base (Metabolic Acidosis): Decreased capacity to excrete acid, leading to an imbalance. Treatable with sodium bicarbonate, but patients are susceptible to severe acidosis; (diarrhea, ketoacidosis).

• Bone Metabolism: Diminished calcium absorption, increased parathyroid hormone, and vitamin D metabolism issues alongside phosphorus retention and acidosis cause bone reabsorption.

• Cardiovascular Issues: Hypertension commonly occurs due to salt/fluid overload, leading to an increased incidence of cardiovascular disease, and is the leading cause of death for CKD patients.

Glomerulonephritis

• Types: Acute (sudden hematuria/proteinuria, reduced GFR, often associated with infections, e.g., Group A streptococci), chronic (persistent abnormalities, gradual decline in renal function, and eventual ESRD), and nephrotic syndrome (significant proteinuria, edema).

• Pathophysiology: Immune-related damage to glomeruli, varying in extent and cause, with potential genetic predisposition and environmental triggers. Antibodies and microscopic examinations assist in classification.

• Consequences: Leakage of blood cells and proteins, fluid/salt retention leading to edema, hypertension and hypoalbuminemia.

Renal Stones

• Presentation: Flank pain that may radiate, microscopic or macroscopic hematuria (blood in urine); possible obstruction, decreased/absent urine production.

• Composition: Primarily calcium. Causes include idiopathic hypercalciuria (high calcium in urine).

• Contributing Factors: Dehydration, high protein/sodium diets.

• Complications: Obstruction complications include hydro-nephrosis, and possible permanent renal damage, infection or abscess, repeated stones contributing to hypertension due to obstructed kidney.