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
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
3
Q
What are the 3 types of intrinsic renal disease?
A
- Glomerular syndromes
- Tubular syndromes
- Vascular syndromes
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
5
Q
What are 2 categories of tubular disease?
A
- Inflammatory tubular interstitial disease (infectious, noninfectious)
- Noninflammatory tubular interstitial disease
- Chronic interstitial disease
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)
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
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)
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)
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
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)
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
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
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
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
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
