Renal Diseases Overview

Renal Diseases

• Renal diseases are a significant health concern.
• The speaker, Muhammad Reihan, is an associate professor of medicine.

Learning Objectives

• Relate pathophysiological basics and etiology of renal diseases.
• Apply the evidence-based approach in managing renal diseases.
• Describe epidemiology, manifestations, complications of renal diseases.

Renal Failure

• Defined as a substantial loss of kidney function, reaching a point where less than 15% of normal glomerular filtration rate (GFR) remains.
• A GFR test, a blood test, assesses kidney function.
• Kidney disease can progress to kidney failure.

Acute and Chronic Renal Failure

• Acute renal failure is potentially reversible.
• Chronic renal failure is a progressive loss of renal function over years, potentially leading to permanent renal failure.
• Chronic renal failure stems from progressive kidney damage and subsequent loss of function.

Stages of Chronic Renal Failure

• Stages of chronic renal failure are categorized into progressive stages based on the loss of GFR.
• The stages include: diminished renal reserve, renal insufficiency, renal failure, and end-stage renal disease.

Causes of Chronic Renal Failure

• Diabetes is the most prevalent cause of chronic kidney disease in developed countries.
• Chronic infections contribute to chronic renal failure.
• Obstructions (prolonged) in the renal system can cause the disease.
• Exposure to toxic chemicals, toxins, and drugs (such as aminoglycoside antibiotics), can cause the disease.
• Hypertension and nephrosclerosis (atherosclerosis of the renal artery) are contributors to the condition.
• Polycystic kidney disease is another potential cause.

Symptoms of Chronic Renal Failure

• Anemia, dry skin, poor appetite, vomiting, bone pain, and metallic taste in the mouth are common symptoms.
• Headaches and the inability to concentrate urine are also observed.
• Increased urination (polyuria) or decreased urination (oliguria) can be present.
• Accumulation of waste products in the blood (azotemia) contributes to symptoms, such as edema, decreased GFR, elevated potassium (serum K), and high blood pressure (BP).
• Weakness and fatigue are frequently reported.

Uremic Stomatitis

• Urea secretion in saliva leads to urease production from oral microflora.
• Free ammonia release damages the oral mucosa.
• Symptoms include painful plaques and crusts on buccal mucosa, dorsum of the tongue, and floor of the mouth.
• Erosions and ulcerations with a gray pseudo-membrane exudate are hallmarks.

Oral Manifestations of Chronic Renal Failure (Uremic Stomatitis)

• Soft tissue changes include bleeding diathesis (petechiae and ecchymosis).
• Irritation and chemical injury to the mucosa due to ammonia compounds cause discomfort.
• Xerostomia, a dry mouth, and an unpleasant taste are symptoms.
• Burning mouth and unpleasant breath odor are often observed.
• Ulcers can result from factors such as anemia, viral infections (immunocompromised individuals), and long-term use of medications like cyclosporine or Nifedepine (CCB).

Hard Tissue Changes in Uremic Stomatitis

• Stained teeth (due to iron supplements) and reduced dental caries (due to saliva urea).
• Delayed tooth eruption and enamel hypoplasia are encountered.
• Tooth mobility is a common consequence, due to alveolar bone resorption, external root resorption, and pain.

Oral Manifestations in Hyperparathyroidism

• Teeth appear more radiopaque against a background of osteoporotic bone.
• Loss of trabeculations (bone structures) in the jaw results in a ground glass appearance.
• There is loss of cortical outlines of the inferior alveolar sinus.
• Pulp calcifications and multilocular radiolucency are often observed.
• Arterial and oral calcification are additional effects.

Treatment of Chronic Renal Failure

• Careful management of fluids, electrolytes, and dietary protein intake are critical.
• Treat anemia, renal dialysis, and renal transplantation are therapeutic approaches as needed.

Post-streptococcal Glomerulonephritis (PSGN)

• Caused by Group A β-hemolytic streptococci (GAHS) serotypes 12, 4, 1.
• Manifestations involve throat infections (pharyngitis/ tonsillitis) or skin infections.
• Symptoms appear weeks after initial infection, with common features including periorbital and peripheral edema, elevated blood pressure, and discoloration of urine (tea or cola-colored).

Pathogenesis of PSGN

• Throat or skin infection by GAHS serotypes leads to production of antibodies against streptococci.
• Antigen-antibody complexes are deposited in glomerular basement membrane.
• This process triggers inflammation, characterized by hematuria (blood in urine), RBC casts in urine, proteinuria, hypertension, oliguria, and azotemia (elevated waste products in blood).

Clinical Features of PSGN

• Usually seen in children (ages 3-12).
• Begins weeks after streptococcal infection (1-2 weeks after pharyngitis/ tonsillitis, or 3-4 weeks after skin infection).
• Edema is a prominent symptom.
• Raised blood pressure is observed.
• Discolored urine (tea/cola color) is a common indicator.

Signs and Symptoms of PSGN

• Edema is a significant symptom, particularly periorbital.
• High blood pressure and lethargy are often observed.
• Proteinuria, hematuria, and oliguria/dysuria (difficulty urinating) are typical.
• Low-grade fever is occasionally reported.

Investigations of PSGN

• Urine analysis assesses for hematuria, proteinuria, and casts.
• Serology tests for streptococcal antibodies and infection.
• Throat swabs are crucial diagnostic measures.
• Renal function tests gauge kidney function.

Treatment of PSGN

• Supportive care with fluid and sodium restriction.
• Diuresis typically occurs within 7-10 days after symptoms onset.
• Antibiotic treatment with penicillin V (10 days) can be employed.

References

• AMBOSS
• Harrison's Principles of Internal Medicine (20th edition) (ISBN-13: 978-1259644030)