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Nephritic Diseases: Causes, Symptoms, and Management, Summaries of Gastroenterology

Tbilisi State Medical UniversityGastroenterology

An in-depth analysis of various nephritic diseases, their causes, symptoms, and management strategies. It covers primary, secondary, and post-infectious glomerulonephritis, iga nephropathy, post-streptococcal glomerulonephritis, anti-glomerular basement membrane disease (goodpasture syndrome), alport syndrome, nephrotic syndrome, minimal change disease, focal segmental glomerulosclerosis (fsgs), and specific secondary causes of nephrotic syndrome, including diabetic nephropathy and amyloidosis.

Typology: Summaries

2018/2019

Uploaded on 02/20/2024

nayana-krishna
nayana-krishna ๐Ÿ‡ฌ๐Ÿ‡ช

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GLOMERULAR SYNDROMES AND GLOMERULOPATHIES
โ€ข Glomerulus โ€“ capillary loop with basement membrane which allows passage of specific
molecules into the nephron
โ€ข inflammatory or noninflammatory diseases of the glomeruli and are associated to a variable
extent with hematuria, proteinuria, hypertension, and a decrease in the GF
โ€ข Can present as nephrotic and/or nephritic syndrome
NEPHRITIC SYNDROME
glomerular capillary damage leading to hematuria, pyuria, water retention, and subsequent
hypertension and edema. It can be caused by a variety of conditions including autoimmune,
hereditary, and infectious diseases. Nephritic diseases can manifest with varying degrees of severity,
ranging from asymptomatic hematuria to systemic involvement, as in rapidly progressive
glomerulonephritis.
CAUSES
โ€ข Primary
โœ“ IgA Nephropathy (Berger's disease)
โœ“ Rapidly progressive glomerulonephritis
โœ“ Membranoproliferative glomerulonephritis
โ€ข Secondary glomerulonephritis
โœ“ Henoch-Schรถnlein purpura
โœ“ Vasculitis-
โœ“ Connective tissue disorders- SLE
โœ“ Churg-Strauss syndrome
โ€ข Post-infectious glomerulonephritis
โœ“ EBV
โœ“ Hepatitis B and C
โœ“ Measles
โœ“ Mumps
โ€ข Hereditary disorders:
โœ“ Alport syndrome
โœ“ Thin basement membrane disease
SYMPTOMS
MAIN
โœ“ Haematuria/ red cell casts- dysmorphic RBC
โœ“ Hypertension (mild)- due to volume overload and suppression of RAAS
โœ“ Oliguria < 500 ml of urine/day
โœ“ Uraemia/ Azotemia
โœ“ Proteinuria (<3g/24 hours)
Flank pain and general systemic symptoms
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GLOMERULAR SYNDROMES AND GLOMERULOPATHIES

  • Glomerulus โ€“ capillary loop with basement membrane which allows passage of specific molecules into the nephron
  • inflammatory or noninflammatory diseases of the glomeruli and are associated to a variable extent with hematuria, proteinuria, hypertension, and a decrease in the GF
  • Can present as nephrotic and/or nephritic syndrome NEPHRITIC SYNDROME glomerular capillary damage leading to hematuria, pyuria, water retention, and subsequent hypertension and edema. It can be caused by a variety of conditions including autoimmune, hereditary, and infectious diseases. Nephritic diseases can manifest with varying degrees of severity, ranging from asymptomatic hematuria to systemic involvement, as in rapidly progressive glomerulonephritis. CAUSES
    • Primary โœ“ IgA Nephropathy (Berger's disease) โœ“ Rapidly progressive glomerulonephritis โœ“ Membranoproliferative glomerulonephritis
    • Secondary glomerulonephritis โœ“ Henoch-Schรถnlein purpura โœ“ Vasculitis- โœ“ Connective tissue disorders- SLE โœ“ Churg-Strauss syndrome
    • Post-infectious glomerulonephritis โœ“ EBV โœ“ Hepatitis B and C โœ“ Measles โœ“ Mumps
    • Hereditary disorders: โœ“ Alport syndrome โœ“ Thin basement membrane disease SYMPTOMS MAIN โœ“ Haematuria/ red cell casts- dysmorphic RBC โœ“ Hypertension (mild)- due to volume overload and suppression of RAAS โœ“ Oliguria < 500 ml of urine/day โœ“ Uraemia/ Azotemia โœ“ Proteinuria (<3g/24 hours) Flank pain and general systemic symptoms

IGA NEPHROPATHY

Presentation: โœ“ Most commonly presents as chronic GN: โœ“ 40% present with gross hematuria. โœ“ 30% are found incidentally with persistent microscopic hematuria. โœ“ May present in association with a concurrent upper respiratory infection โœ“ Presents much less commonly as acute GN or RPGN (approximately 5%โ€“10%) Diagnosis: โœ“ Labs: normal serum complement levels โœ“ Kidney biopsy findings: ๏€ช Light microscopy: mesangial hypercellularity ๏€ช Immunofluorescence: positive for IgA in the mesangium ๏€ช Electron microscopy: mesangial immune deposits Management: ๏€ช Observation if creatinine is normal and proteinuria is < 500 mg/day ๏€ช ACEi if proteinuria is 500 mgโ€“1000 mg/day ๏€ช Steroids for progressive disease ๏€ช Transplantation if progression to end-stage renal disease (ESRD) POSTSTREPTOCOCCAL GLOMERULONEPHRITIS Presentation:

  • Most common cause of acute nephritic syndrome (but not concurrently) in children
  • Can present 1โ€“3 weeks after a throat infection caused by specific nephritogenic strains of group A beta-hemolytic Streptococcus
  • Can present 3โ€“6 weeks after a skin infection (impetigo): caused by group A Streptococcus or Staphylococcus aureus Diagnosis: Labs: โœ“ Streptozyme test: measures 5 different antibodies including antistreptolysin-O after pharyngeal infection โœ“ Urinalysis: hematuria with RBC casts, +/โ€“ proteinuria Kidney biopsy findings: โœ“ Light microscopy: diffuse endocapillary proliferation with neutrophils โœ“ Immunofluorescence: C3 positive; granular IgG โ€œlumpy-bumpyโ€ or โ€œstarry skyโ€ pattern โœ“ Electron microscopy: subepithelial โ€œhump-likeโ€ immune complex deposits Management: Supportive care โœ“ Antibiotics: only if the strep infection is still present at the time of diagnosis โœ“ Treat hypertension and/or edema: Loop diuretics (e.g., furosemide), Sodium and water restriction

CLASSIFICATION

  • Primary - specific to kidney disease โœ“ Minimal change disease- MC cause in children โœ“ Focal segmental glomerulosclerosis- in adults โœ“ Membranous nephropathy โœ“ Mesangial proliferative glomerulonephritis
  • Secondary - renal manifestation of systemic general illness

โ€ข Metabolic causes:

โœ“ Diabetes mellitus

โœ“ Amyloidosis

โ€ข Immunological- SLE, Sjogrenโ€™s syndrome

โ€ข Idiopathic- sarcoidosis

โ€ข Drug related- NSAIDS

โ€ข Infectious- Hepatitis

โ€ข Genetic- sickle cell disease

MAIN- Classic clinical presentation of nephrotic syndrome: โ– Greater than 3.5 g/day proteinuria โ– Urine microscopy may show signs of lipiduria : โ– โ€œOval fat bodiesโ€ or fatty casts on light microscopy โ– โ€œMaltese crossโ€ on polarized light microscopy โ– Hypoalbuminemia- albumin loss , Low serum albumin โ†’ low plasma oncotic pressure โ†’ fluid shifts from plasma volume to interstitial space โ†’ low effective circulating volume (ECV) โ†’ stimulates RAAS โ†’ Na+ retention โ†’ water retention Na+ and water retention + sympathetic stimulation + reduced natriuretic peptide release โ†’ pitting edema โ– Peripheral/periorbital edema โ– Hyperlipidemia- Decreased oncotic pressure โ†’ hepatic lipoprotein synthesis โ†’ hyperlipidemia โ– Serum creatinine is often normal. SYMPTOMS

  • Weight gain
  • Puffiness of face (facial edema esp around eyes - apparent when wake up and subsides during the day)
  • Frothy urine with fatty casts
  • Abdominal swelling
  • Low urine output/oliguria
  • Fatigue
  • Pitting edema
  • Hypertension INVESTIGATIONS
  • Urine dipstick- to confirm proteinuria
  • Urinalysis- 3+, 4+
  • CBC
  • 24 hr urine collection- to assess g/day protein excretion.
  • Proteinuria >3.5g/day or UPC ratio >
  • Serum creatinine test - to rule out ARF, assess GFR
  • Serum albumin and cholesterol levels
  • Lipid panel for hyperlipidemia
  • Renal biopsy and USS Management All etiologies of nephrotic syndrome share similar treatment measures; secondary etiologies also need to have the underlying causes addressed. Dietary Na+ restriction: 2 g/day Strict blood pressure control: โœ“ Goal < 130/80 mm Hg โœ“ Helps reduce proteinuria โœ“ Helps reduce the progressive loss of glomerular function ACEis or angiotensin-receptor blockers (ARBs): โœ“ Decrease proteinuria by reducing glomerular capillary pressure โœ“ Treat systemic hypertension- Lisinopril (ACEi), Losartan (ARB) SGLT2 inhibitors: โœ“ Decrease proteinuria โœ“ May benefit individuals with CKD and proteinuria (even without a diagnosis of diabetes) Loop diuretics: โœ“ Reduce hypervolemia and decrease edema โœ“ May cause hypovolemia if serum albumin is very low, Furosemide Statin (HMG-CoA reductase inhibitor) for hyperlipidemia: โœ“ May not be needed if improved with disease treatment โœ“ Examples of drugs used: โœ“ Atorvastatin โœ“ Simvastatin MINIMAL CHANGE DISEASE
  • Presentation:
  • Abrupt onset more often than other nephrotic diseases
  • Can have some nephritic features also (microscopic hematuria)
  • Can present with AKI
  • Rarely causes end-stage renal disease (ESRD) Etiologies:
  • Primary : idiopathic

Management: All cases: โœ“ ACE โœ“ Loop diuretic โœ“ Dietary Na+ restriction โœ“ Statin for hyperlipidemia (if not improved with disease treatment) FOCAL SEGMENTAL GLOMERULOSCLEROSIS (FSGS) Focal segmental glomerulosclerosis is a histologic lesion commonly found in individuals with nephrotic syndrome rather than a specific disease entity. Etiologies: โœ“ Primary (idiopathic): presents with classic nephrotic syndrome โœ“ Secondary: often presents with nonโ€“nephrotic-range proteinuria due to: โœ“ Decreased nephron mass in solitary kidney โœ“ Recurrent kidney injury due to reflux nephropathy or sickle cell disease โœ“ Progressive CKD from any etiology โœ“ Most important viral cause: HIV โœ“ Drugs: pamidronate, interferon, heroin โœ“ Genetic causes: may present at any age Biopsy findings of FSGS should prompt an evaluation to determine the underlying cause: โœ“ Light microscopy: segmental sclerosis โœ“ Immunofluorescence: nonspecific โœ“ Electron microscopy: foot process effacement localized to regions of segmental sclerosis Management: โœ“ Primary: General measures (ACEi, statin, loop diuretic, low-Na+ diet) โœ“ High-dose steroid with a long taper โœ“ Steroid-dependent with relapses โ†’ cyclophosphamide โœ“ Steroid-resistant โ†’ cyclosporine + prednisone or mycophenolate mofetil โœ“ Resistant to all therapies suggests misdiagnosed genetic FSGS โ†’ transplantation SPECIFIC SECONDARY CAUSES OF NEPHROTIC SYNDROME Diabetic nephropathy: โœ“ Most common cause of nephrotic-range proteinuria โœ“ 20%โ€“30% of all individuals with diabetes will develop some stage of CKD. โœ“ Most common overall cause of ESRD (approximately 55% of all individuals new to dialysis) Presentation: progresses from microalbuminuria to nephrotic proteinuria over many years Diagnosis is based on kidney biopsy if the presentation is not classic: โœ“ Characteristically shows Kimmelstiel-Wilson nodules โœ“ Can coexist with other nephrotic diseases (such as MCD, membranous nephropathy, and FSGS) Treatment:

โœ“ Strict glycemic control and ACEi โœ“ Additional renal-protective medications: โœ“ Sodium-glucose cotransporter 2 (SGLT2) inhibitors โœ“ Nonsteroidal selective mineralocorticoid receptor antagonists (MRAs) โœ“ Possible transplantation AMYLOIDOSIS: Relatively rare cause of nephrotic syndrome Presents with nephrotic-range proteinuria (> 3.5 g/day) Diagnosis : โœ“ SPEP with immunofixation (IFE) โœ“ UPEP โœ“ Biopsy findings: โœ“ Light microscopy: apple-green birefringence on polarized microscopy with Congo red stain โœ“ Electron microscopy: amyloid fibrils Treatment: โœ“ ACEis โœ“ Loop diuretic โœ“ Dietary Na+ restriction โœ“ Statin for hyperlipidemia โœ“ Prognosis: high risk of progression to ESRD