Renal Syndromes: Wall Flashcards

1
Q

What are 4 things you might use to diagnose abnormal kidney function?

A
  • Changes in serum creatinine concentration
  • Abnormalities in urinalysis
  • Altered renal homeostatic mechanisms
  • Abnormal kidney imaging studies
  • NOTE: these are routine things that anyone in any office practice will have access to
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2
Q

What are the important diagnostic categories of kidney disease?

A
  • Acute or chronic process
  • Pre-renal, intrinsic renal, or post-renal origin
  • Glomerular, tubular, or vascular origin
  • Inflammatory or noninflammatory process
  • Associated with underlying systemic disease
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3
Q

What are the 3 types of intrinsic renal disease?

A
  • Glomerular syndromes
  • Tubular syndromes
  • Vascular syndromes
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4
Q

What are 5 different categories of glomerular disorders?

A
  • Nephrotic syndrome
  • Nephritic syndrome
  • Mixed nephritic nephrotic syndrome
  • Mesangial nephritic syndrome
  • Chronic glomerular disease
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5
Q

What are 2 categories of tubular disease?

A
  • Inflammatory tubular interstitial disease (infectious, noninfectious)
  • Noninflammatory tubular interstitial disease
  • Chronic interstitial disease
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6
Q

What are 4 categories of vascular kidney syndromes?

A
  • Prerenal azotemia
  • Renal artery stenosis (unilateral or bilateral)
  • Hypertensive nephrosclerosis
  • Vasculitis involving the kidney
    1. Typically present as nephritic syndrome
    2. Reduced GFR, hematuria, proteinuria (usually in the non-nephrotic range)
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7
Q

Describe nephrotic syndrome, and some of its characteristic features.

A
  • Abnormal permeability of glomerular capillary wall to protein -> proteinuria/albuminuria
  • Features: proteinuria, lipiduria (may see fatty casts)
    1. Typically > 3 g/day; random urinary protein to creatinine ratio >3 (spot urine)
    2. 3+-4+ (highest) UA dipstick for protein
    a. Dipstick urines detect albumin b/c (-) charge -> only recognizes (-) proteins
    3. Low serum albumin: low oncotic pressure
    4. Peripheral edema: expanded interstitial volume bc most Na, water retention there (no expansion of IV volume)
    5. Typically normal GFR and normal BP
  • NOTE: may not have all of these things, but still have glomerular disease
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8
Q

What are some clinical examples of nephrotic syndrome?

A
  • Minimal change (children; 10-15% of adults) -> MCD
  • Focal segmental glomerulosclerosis (a little bit more common in AA; Apo L1) -> FSGS
  • Membranous glomerulopathy (most common in Caucasian) -> MN
  • Diabetic nephropathy: most common etiology of nephrotic syndrome (due to systemic disease) -> most common cause of proteinuria, CKD, etc.
    1. B/c there are so many more T2D than T1D, #’s are much more prevalent in the T2 population
    2. Different than other 3 b/c by the time you are overtly nephrotic, GFR is DEC and pt has HTN (others have normal GFR and BP early on)
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9
Q

Is nephrotic syndrome associated with volume changes?

A
  • Direct renal tubular retention of salt and water in the distal tubule -> plasmin gets filtered when there is heavy proteinuria, altering activity of ENaC
  • Expanded total body sodium and total body water
  • Expanded interstitial fluid volume (edema)
  • Due to low serum albumin, going to favor more salt and water in the interstitial compartment (i.e., may not be ¾th, 1/4th relationship)
  • Relatively normal plasma volume (normal BP)
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10
Q

Nephritic syndrome basics

A
  • Inflammatory changes in glomerulus -> infiltration of glomerulus by inflammatory cells
  • Endothelial cell swelling
  • Complement activation, often present
  • Losing capillary surface area, so you are going to have a drop in GFR
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11
Q

What are the urinary findings in nephritic syndrome?

A
  • Hematuria (micro or gross hematuria): HALLMARK of mesangial inflammation
  • Dysmorphic red blood cells in urine
  • RBC casts (Tamm Horsfall) -> PATHOPNOGMONIC
  • Non-nephrotic ranged proteinuria (<2 g/d or urinary protein creatinine ratio <2), 1+-2+dipstick for protein (less positive for protein than w/nephrotic syndrome)
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12
Q

What are the clinical features of nephritic syndrome?

A
  • HTN: retained salt and water, but they have not lost oncotic pressure (plasma volume has built up) -> pulmonary edema
  • Reduced GFR (glomerular filtration rate)
  • Possible gross hematuria: urine may be tea-colored or look like Coca-Cola
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13
Q

What volume changes are associated with nephritic syndrome?

A
  • Renal retention of salt and water: mainly because of acute reduction of GFR
  • Expanded total body sodium and total body water, but still in 3/4th, 1/4th distribution
  • Expanded ECFV, expansion of both EC and IC fluid spaces (depending on changes in osmolality)
    1. Won’t change IC volume w/o change in osmolality
  • Hypertension and possible pulmonary edema
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14
Q

What are some clinical examples of nephritic syndrome?

A
  • Post-strep glomerulonephritis (post-infectious glomerulonephritis): prototype for a pure nephritic process
  • Infection-associated glomerulonephritis
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15
Q

What is the mesangial nephritic pattern? What is its hallmark?

A
  • Glomerular inflammatory changes restricted to the mesangial area of the glomerulus
  • Glomerular capillary wall (capillary loops) remains unaffected: ~normal GFR, minimal proteinuria
  • Hallmark is hematuria (microscopic or sometimes gross hematuria)
  • Red cell casts due to glomerular inflammation
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16
Q

What are some clinical examples of mesangial nephritis?

A
  • IgA nephropathy (most common glomerulonephritis worldwide): prototype for this pattern of something really only injuring the mesangium
    1. In some places, like SE Asia, this is one of the leading causes of CKD
  • Systemic lupus erythematosus with immune deposits restricted to the mesangium
    1. SLE class II CKD
17
Q

What is mixed nephrotic/nephritic syndrome? Provide some examples.

A
  • Evidence for inflammatory glomerular disease (hematuria, reduced GFR) AND nephrotic range proteinuria (low serum albumin and edema formation)
    1. Low GFR, elevated serum creatinine
  • Diffuse proliferative glomerulonephritis related to SLE (class IV lupus)
  • Membranoproliferative glomerulonephritis (MPGN), most often related to hepatitis C (cryoglobulins)
18
Q

What is chronic glomerular disease? Provide some examples.

A
  • Chronically abnormal GFR (elevated serum creatinine) and chronically abnormal UA
    1. Most often detected based on previous data
  • Variable degrees of proteinuria and hematuria; may not be in very high quantities
  • Frequently leads to decreased sized kidneys
    1. Usually measured by ultrasound (bilaterally decreased in size, with increased echogenecity)
  • Progressive scarring in interstitium and glomerulus
  • Waxy casts: dilated cast in tubules -> CHRONICITY
  • Examples:
    1. Diabetic nephropathy
    2. Long-standing intrinsic glomerular disease, i.e., membranous glomerulopathy, FSGS, IgA nephropathy
19
Q

What is non-inflammatory tubulointerstitial disease? Provide some examples.

A
  • Reduced GFR (acute renal failure)
  • Impaired concentrating and diluting ability
    1. Isosthenuric urine, osmolality ~300 mosm/kg, specific gravity ~1.010 (on UA)
    2. Impaired sodium conservation (FENa >1%)
  • Urinalysis: granular casts (hyaline casts w/granular material in them), relative absence of inflammatory cells and red blood cells
  • Minimal proteinuria (<1.0 g/d) since glomerulus fine, but tubules are injured
  • Examples:
    1. Acute tubular necrosis (ATN)
    2. Prolonged ischemia- hypoxia (most common )
    3. Direct nephrotoxins: aminoglycosides (selectively taken up by tubules -> lysosome injury), amphotericin B, heavy metals, IV iodinated contrast media, myoglobin (iron injures tubules), free hemoglobin
  • Inflam cells not req’d to produce tubular damage; come in to repair things, but not initiating problem
20
Q

What is inflammatory tubulointerstitial injury? Provide some examples.

A
  • Similar to non-inflammatory tubular damage except active inflam response results in tubular damage
    1. Allergic interstitial nephritis (drug acting like a hapten, causing direct injury to tubules)
    2. Graft rejection
  • UA: sterile pyuria, often eosinophils in the urine (Hansel’s or Wright’s stain)
    1. NEUTROPHILS (WBC’s in urine)
  • Recent creatinine drop + recent exposure to new drug
  • Most commonly due to drugs: beta-lactam AB’s, sulfa derived antibiotics, dilantin, allopurinol
    1. May be assoc w/viral infections (legionella), but uncommon -> mostly drug-induced
21
Q

What is acute pyelonephritis?

A
  • Acute bacterial infection, ascending route, most commonly gram-negative bacilli (urinary cultures are positive, usually for E. Coli)
  • Inflam damage in medulla, pus in inner medulla
  • Urinary findings: bacteria, pyuria, maybe WBC casts
    1. Neutros can get incorporated into the casts
    2. If you see casts, you know kidney is involved, and not just bladder
  • Not everyone with pyelonephritis looks terribly ill
22
Q

What is obstructive uropathy? Provide some examples.

A
  • Leads to tubular damage; may be acute or chronic
  • Impaired tubular function (impaired: concentrating ability, Na conservation, and K+ secretion)
  • Frequently hyperkalemia and metabolic acidosis as a consequence of damage to collecting duct
  • Minimal proteinuria
  • Imaging studies are necessary to define etiology
  • Examples:
    1. Benign prostatic hypertrophy or prostate cancer (bladder outlet obstruction)
    2. Gynecological malignancies with bilateral ureteral obstruction
    3. Nephrolithiasis (stones)
23
Q

What is chronic tubulointerstitial disease? Provide some clinical examples.

A
  • Chronically decreased GFR (elevated serum creatinine concentration)
  • Impaired concentrating ability => NOCTURIA
  • Minimal proteinuria, <1 gm/d
  • Waxy casts: simply signify chronic disease
  • Decreased kidney size by imaging studies (ultrasound); more echogenic
  • Just means whatever tubular injury process started has become chronic
24
Q

What is pre-renal azotemia, and what are the associated lab findings?

A
  • Can be a cause of acute renal failure
  • Kidneys are normal: hyaline casts (only normal cast)
  • Due to impaired renal perfusion pressure or severely decreased renal blood flow
  • Lab findings:
    1. Normal urinalysis
    2. BUN/Creatinine ratio >20 (DEC RPF, DEC GFR, INC urea reabsorb, INC creatinine secrete)
    3. Concentrated urine (osmolality >500 mosm/kg), specific gravity >1.020
    4. FENa<1%
    5. Kidney imaging studies are normal
25
Q

What are some clinical examples of pre-renal azotemia? What things might aggravate it?

A
  • Examples:
    1. Low cardiac output: CHF, cardiac tampanode, arrhythmias (severely DEC or INC HR)
    2. Hemorrhage
    3. ECFV deficit (vomit, diarrhea, severe de-H2O)
  • Degree of acute renal failure exacerbated by drugs that** impair RAS b/c they **disrupt glomerular auto-reg
  • Impede ability to keep GFR normal (can do this with NSAIDs or ACEI/ARBs)
    1. NSAIDs: reduced renin secretion, reduced vasodilatory prostaglandin production
    2. ACEI/ARB: impaired angiotensin II production or response to AII
26
Q

What is renal artery stenosis?

A
  • Unilateral: lots of ANG II and aldosterone -> healthy kidney will compensate, raising GFR, so you may not see much effect on total GFR
    1. HTN will cause pressure natriuresis in normal kidney, INC Na excretion -> euvolemic HTN; NOT edematous due to pressure natriuresis
    a. HTN exquisitely sensitive to RAS
    b. Can get hypertensive nephrosclerosis in healthy kidney
  • Bilateral stenosis: ACE/ARB can precipitate acute renal failure by disrupting glomerular autoregulation
    1. Edema and HTN (volume expansion)
27
Q

What is hypertensive nephrosclerosis?

A
  • Medial hypertrophy of renal arterioles (medium, sm arteries) -> leads to ischemic glomerular atrophy
  • DEC # of functioning nephrons = DEC GFR
  • Non-inflammatory: absence of hematuria, pyuria
  • Low-grade proteinuria or (-) for proteinuria, <1gm/dn
  • 2nd most common cause of ESRD; can cause CKD
    1. More common in AA (abnormal Apo L1 allele)
  • Bilaterally symmetrically decreased sized kidneys
  • Very bland UA
28
Q

What is malignant HTN?

A
  • Severely elevated BP (way over 200 systolic)
  • Onion-skinning
  • Acutely damaging arterioles and capillaries
  • Can present with acute renal failure
  • Can result in proteinuria and microscopic hematuria
    1. Life-threatening unless HTN urgently controlled
    2. Looks kinda like thrombotic microangiopathy
29
Q

What is vasculitis in the kidney? Provide some clinical examples.

A
  • Typically present as nephritic syndrome
  • Reduced GFR, hematuria, proteinuria (usually in the non-nephrotic range)
  • Examples:
    1. Thrombotic microangiopathies: hemolytic uremic syndrome (hemolytic anemia, thrombocytopenia, abnormal renal function)
    2. Polyarteritis nodosa: segmental infarcts by wiping out arcuate arteries
    3. ANCA associated vasculitis (pauci-immune)
    4. Malignant hypertension
30
Q

What is rapidly proliferative glomerulonephritis (RPGN)?

A
  • Just means inflammatory glomerular process that is tearing up the kidney in a matter of days to weeks -> untreated will lead to permanent kidney loss and requirement of renal replacement therapy
    1. Decreased GFR over weeks to months
  • Immune complex mediated: hep C, MPGN, class IV Lupus
  • Anti-GBM antibody
  • Pauci-immune: NO Ig on IF or dense deposits on EM
    1. Usually assoc w/ANCA’s (not circulating in complexes, so not clogging up glomeruli, but are injuring endo) -> nephritic appearance
  • FSGS: segments will necrotize and rupture
  • Crescent formaton: almost a synonym for RPGN
  • REMEMBER: Need to be able to correlate urinary findings w/clinical syndromes -> most clinically helpful tool besides history is what’s going on in UA