Pathology: Urinary (short)

Normal Renal Function

• Upper urinary tract comprises the kidneys and ureters; Lower urinary tract consists of the bladder and urethra.
• Kidney anatomy includes:
  • Cortex: outer layer with glomeruli and convoluted tubules.
  • Medulla: inner layer housing the loop of Henle and collecting ducts.
• Collecting ducts converge into lobes, which may form single or multiple papillae depending on species.
• Blood enters kidneys via renal artery; renal arterioles pass through glomeruli for filtration.

Nephron Function and Urine Concentration

• Nephrons consist of glomerulus and tubules; filtration barrier keeps large molecules (cells, proteins) from entering urine.
• Filtration is driven by blood pressure, allowing small, soluble, or negatively charged substances through.
• Urine concentration mechanisms:
  • Hypertonic medulla: promotes water movement into interstitial space.
  • Collecting duct: ADH (antidiuretic hormone) increases water reabsorption.
• Optimal concentrated urine requires functional nephrons, ADH, and a hypertonic medulla.
• Functional reserve allows for the loss of up to two-thirds of nephrons without affecting renal function; >75% loss leads to renal failure.

Kidney Functions

• Maintains body fluid balance.
• Excretes metabolic waste, especially from protein breakdown.
• Regulates electrolytes (PO4, K, Na).
• Produces hormones like erythropoietin (EPO).

Kidney Dysfunction

• Dysfunctions manifest as inability to concentrate urine, excrete waste, regulate electrolytes, or produce EPO.
• Critical thresholds for urine concentrating ability:

  • 66% damage: Inability to concentrate urine.

  • 75% damage: Failure to maintain fluid balance.

• Urine concentration measured via specific gravity:
  • Isosthenuric: 1.008 - 1.012.
  • Hyposthenuric: >1.012.

Altered Excretion Patterns

• Azotemia indicates impaired urea and creatinine clearance due to nephron damage.
• Hyperphosphatemia occurs with renal failure due to phosphate retention.
• Potassium levels vary with kidney function: more excretion with high flow rates, leading to hypokalemia; conversely, low flow rates cause hyperkalemia.

Diagnostic Indicators of Renal Failure

• Symptoms include polydipsia/polyuria or oliguria/anuria, isosthenuria, azotemia, hyperphosphatemia, and anemia.
• Collectively referred to as uremia.

Azotemia Classification

• Pre-renal: Dehydration reduces blood flow to kidneys, causing oliguria and concentrated urine.
• Renal: >75% nephron damage leads to decreased urea/creatinine excretion and less concentrated urine.
• Post-renal: Obstruction leads to reabsorption of waste products into blood.
• Non-renal: Increased protein breakdown from various conditions.

Conditions Affecting the Upper Urinary Tract

• Congenital abnormalities include renal aplasia, hypoplasia, dysplasia, and ectopic kidneys.
• Vascular conditions: Embolic glomerulitis and interstitial nephritis due to infections (e.g., Leptospirosis).
• Chronic interstitial nephritis leads to CKD, characterized by fibrosis and enlarged, firm kidneys.

Tubular and Medullary Diseases

• Tubular disease can be inflammatory or necrotizing, caused by ischemia or toxins.
• Oxalate-containing plants and ethylene glycol cause acute kidney injury through crystal formation.
• Pyelonephritis arises from lower tract infections ascending to the renal pelvis.

Lower Urinary Tract Disease and Lesions

• Congenital defects, such as ectopic ureters and patent urachus, can lead to infections and other complications.
• Cystitis results from inflammation often caused by uropathogens; predisposing factors include trauma and urine pH changes.
• Urolithiasis involves the formation of urinary calculi, with common types varying by species.

Urinary Tract Obstruction

• Most obstructions occur at the urethra, often due to uroliths or plugs.
• Common in males, especially with long urethras; may lead to severe complications if untreated.

Feline Lower Urinary Tract Disease (FLUTD)

• A syndrome characterized by symptoms of cystitis, with multiple potential causes including idiopathic cystitis, urolithiasis, bacterial cystitis, and neoplasia.

Urinalysis

• Cystocentesis is the preferred method for urine sample collection.
• Use of specific gravity (USG) assists in assessing kidney function; normal values depend on hydration status.
• Urine chemistry tests provide insights into protein, glucose, bilirubin, and blood presence.

Proteinuria Interpretation

• Assess protein levels to differentiate between pre-renal, renal, and post-renal causes.
• UPCR used for distinguishing renal disease: <0.5 normal; >1 indicates glomerular disease.

Glucosuria and Bilirubin

• Presence of glucose indicates hyperglycemia, often from diabetes or stress.
• Bilirubin in urine suggests possible cholestatic liver disease, notably in cats.

Importance of the Hypothalamic-Pituitary-Renal Axis

• ADH regulates urine concentration; dysfunction can lead to primary polyuria or polydipsia.### Lack of ADH Production
• Lesions in the pituitary gland lead to a lack of Antidiuretic Hormone (ADH) production; this is uncommon.
• Acquired conditions in dogs often stem from trauma, while cats may have space-occupying lesions.
• Diagnosis often relies on exclusion methods; a positive response to synthetic ADH confirms the condition.

Abnormal Response to ADH

• Abnormalities in the renal distal tubules and collecting ducts result in decreased responsiveness to ADH.
• Reduced response leads to decreased water reabsorption and polyuria, which can be classified as primary or secondary.
• Primary nephrogenic diabetes insipidus occurs when urine concentration does not exceed a specific gravity (SG) of 1.007, even after dehydration; this rare condition manifests early in life.
• Secondary causes include:
  • Hypercalcemia: high serum calcium impedes ADH action.
  • E. coli endotoxins: these toxins reduce ADH sensitivity at the collecting duct but have reversible effects.

Structural Damage to Nephrons

• Significant damage occurs once two-thirds of functional nephrons are compromised; resulting urine specific gravity (USG) becomes isosthenuric or minimally concentrated.

Osmotic Diuresis

• Elevated levels of osmotically active substances in the tubular filtrate inhibit normal water resorption, leading to diuresis.
• Diabetes mellitus is a common cause; excess glucose remains in urine, retaining water as a consequence.

Decreased Medullary Hypertonicity

• Lowered levels of urea and sodium diminish medullary concentration due to:
  • Decreased urea production associated with liver diseases.
  • Increased renal blood flow, often due to prolonged polyuria from fluid overload.
  • Systemic hyponatremia affecting overall sodium levels.

Approach to Diagnosing PU/PD

• Begin with a comprehensive history and physical examination.
• Confirm polydipsia by measuring water consumption over 24 hours, ideally in a normal home setting.
• Conduct a diagnostic screen including urinalysis, hematology, and biochemistry.
• Implement specific tests as necessary, such as T4 and ACTH measurements.

Most Common Causes of PU/PD

• Renal disease.
• Diabetes mellitus.
• Hyperthyroidism, particularly in cats.
• Hypercalcemia from various causes, including malignancies.
• Cushing's disease (hyperadrenocorticism).
• Pyometra, prostatitis, and urinary tract infections.

Test your knowledge on the anatomy and function of the renal system, including the structure of the upper and lower urinary tracts. This quiz covers important components such as the cortex, medulla, blood supply, and lobes of the kidneys. Ensure you understand kidney anatomy and its significance in overall renal function.