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Renal Syndromes by Mind Map: Renal Syndromes

1. Glomerular Syndromes

1.1. Nephritic Syndrome

1.1.1. Features Inflammatory Change in the Glomerulus Decreased GFR Leads to Salt and Water Retention Hematuria Red Blood Cell Casts Small amounts of Proteinuria

1.1.2. Examples Poststreptococcal glomerulonephritis C3 will be low, C4 will be normal Rapidly progressive glomerulonephritis (RPGN)

1.2. Nephrotic Syndromes

1.2.1. Symptoms Lipiduria Proteinuria (> 3 g/day) Hypoalbuminemia Edema

1.2.2. Examples Diabetic Neuropathy most common overall in Adults Non-Inflamitory Visceral Epithelial Injury: Podocytopathies Focal Segmental Glomerular Sclerosis Minimal Change Disease Sub-epithelial Immune Complex Deposit Membranous Glomerulopathy Post-infectious Glomerulonephritis

1.3. Mesangial nephritic pattern

1.3.1. Features Hematuria

1.3.2. Examples IgA Nephropathy SLE Nephropathy

1.4. Mixed nephritic nephrotic syndrome

1.4.1. Features Decreased GFR Hematuria Nephrotic Range Proteinutia Hypoalbuminemia Edema

1.4.2. Examples SLE Nephritis Diffuse Proliferative Glomerulonephritis Membranoproliferative Glomerulonephritis Type I Type II

1.5. Chronic Glomerular Disease

1.5.1. Features Decreased Number of Functioning Nephrons Increased serum Creatinine Chronic proteinuria of Varying degrees Chronic renal insufficiency frequently leads to decreased size kidneys. Chronic Hematuria of Varying Degrees Waxy Casts are unique to chronic Kidney Disease

1.5.2. Examples CKD

2. Tubular Syndromes

2.1. Noninflammatory tubulointerstitial disease

2.1.1. Pathophysiology Renal Tubule fails to reabsorb Glomerular filtration decreases Increased pressure in the Tubules

2.1.2. Clinical Findings Acute Decrease in GFR Increase in serum Creatinine

2.1.3. Urinanalysis Urinary specific gravity is typically 1.010, corresponding to urine osmolality of ~ 300mosm/kg, which is similar to plasma osmolality Damaged Tubules can neither concentrate nor dilute urine Granular Casts are a Hallmark Feature

2.1.4. Examples Acute Tubular Necrosis Ischemia Toxins

2.2. Inflammatory tubular interstitial injury

2.2.1. Urinary Findings Urinary specific gravity is typically 1.010, corresponding to urine osmolality of ~ 300mosm/kg, which is similar to plasma osmolality positive leukocyte esterase microscopic hematuria sterile pyuria (absence of bacteria)

2.2.2. Examples Acute kidney transplant rejection . In this case the allograft is recognized as foreign antigen and an immune response is directed against the renal tubular cells which express histocompatibility antigens. allergic interstitial nephritis some of the infiltrating cells are eosinophils Causitive Agents

2.3. Acute pyelonephritis

2.3.1. Urinary Findings leukocyte esterase positive frequently nitrite positive frequently positive for blood (blood is from the urinary tract rather than kidney) marked pyuria white blood cell clumps bacturia (Urine Cultures will be positive) White Blood Cell Casts

2.4. Obstructive Uropathy

2.4.1. isosthenuric urine

2.4.2. fractional excretion of sodium typically will be > 1%

2.4.3. Patients frequently report voiding symptoms related to bladder outlet obstruction

2.4.4. Urinary finding Minimal Proteinuria Variable Hematuria

2.4.5. DDx Imaging studies are essential

2.5. Chronic interstitial renal disease

2.5.1. Examples analgesic nephropathy chronic pyelonephritis chronic obstructive uropath chronic cyclosporine toxicity chronic lithium toxicity

3. Vascular syndromes

3.1. Prerenal Azotemia

3.1.1. Causes Anything Causing Hypovolemia Decreased Systolic Function Valvular Disease

3.1.2. Urinary Findings Increased Specific Gravity Increased Osmolality

3.1.3. Lab Findings Increased BUN to Creatinine Ratio Serum creatinine is a function of GFR. BUN is a function of GFR and urinary flow rate.

3.2. Renal Artery Stenosis

3.2.1. Leads to Renin Dependent Hypertension

3.2.2. Unilateral Renal Artery Stenosis Treat with ACE or ARB Urinary findings are usually normal in unilateral renal artery stenosis.

3.2.3. Bilateral Renal Artery Stenosis Drugs which interfere with autoregulation in this setting will often precipitate acute renal failure.

3.3. Hypertensive Nephrosclerosis

3.3.1. long-term uncontrolled hypertension leads to arteriolar nephrosclerosis in the microcirculation of the kidney. These progressive changes can lead to ischemic atrophy of glomeruli, and therefore decreased GFR

3.3.2. There is strong association between hypertensive nephrosclerosis and being homozygote for ApoL1

3.3.3. Urinary findings nonnephrotic ranged proteinuria, typically < 1 gram daily

3.4. Renal Vasculitis

3.4.1. ANCA associated RPGN

3.4.2. Polyarteritis Nodosa

3.4.3. Hemolytic Uremia Syndrome the primary pathologic defect is marked glomerular endothelial cell swelling and damage with platelet thrombi formation within the lumens of glomerular capillaries