Chapter 20: The Kidney - Tubular/interstitial Dz/Vascular Dz Flashcards
Which stain is used to view Chronic Glomerulonephritis?
What’s seen?
- Massone trichrome stain
- Showing complete replacement of all glomeruli by blue-staining collagen
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90% of what type of glomerulonephritis will progress to chronic GN?
Other forms of GN that may progress?
- Crescentic GN (90%)
- Membranous nephropathy
- FSGS
- Membranoproliferative GN
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As glomeruli progressively become obliterated in chronic GN, what happens to GFR and protein loss?
- GFR decreases
- Protein loss in urine diminshes
What is the characteristic morphological features of the glomerular lesions associated with SLE (lupus nephritis)?
What is seen on light microscopy and electron microscopy?
- SUBendothelial immune complex deposition + mesangial deposition
- GBM shows “wire loops” of capillaries on light microscopy
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What are the 2 major processes that play a key pathophysiologic role as diabetic glomerular lesions develop?
- Metabolic defect linked to hyperglycemia and advanced glycosylation end products produced thickened GBM and increased mesangial matrix
- Hemodynamic effects associated w/ glomerular hypertrophy also contribute to the development of glomerulosclerosis
What are the 3 major morphological changes seen in diabetic glomerulosclerosis?
- Diffuse capillary BM thickening
- Diffuse mesangial sclerosis
- Nodular glomerulosclerosis****
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In the US, what is the leading cause of end-stage renal disease, adult-onset blindness and non-traumatic LE amputations?
Diabetes
What are the major characteristics of Henoch-Schonlein Purpura?
Who does it most typically affect and onset when?
- Most common in children btw 3-8 yo, often follows a URI
- Purpuric skin rashes on extensor surfaces of arms and legs
- Abdominal pain and vomiting —> intestinal bleeding
- Arthralgias
- Renal abnormalities - microscopic hematuria, mixed or isolated nephritic/nephrotic syndrome
Pathognomonic feature of Henoch-Schonlein Purpura seen on fluorescence microscopy?
Deposition of IgA, sometimes w/ IgG and C3, in mesangial region
What is the morphology of the skin lesions seen in Henoch-Schonlein Purpura?
- Subepidermal hemorrhages and necrotizing vasculitis involving smaller vessels of the dermis
- Deposition of IgA, along w/ IgG and C3 present in the vessels
Which 4 systemic diseases are associated w/ Nephrotic Syndrome?
- Diabetic nephropathy
- SLE
- Hepatitis C - Cryoglobulinemia: Membranoproliferative Type I
- HIV nephropathy: FSGS
Which 4 systemic diseases are associated w/ Nephritic Syndrome?
- SLE = 60-70% pts
- Bacterial endocarditis: acute proliferative GN
- Goodpasture Syndrome: RPGN
- Henoch-Schonlein Purpure (HSP): IgA nephropathy
What are the 3 major renal lesions prototypical of Diabetic Nephropathy?
- Glomerular lesions
- Vascular lesions, principally artriolosclerosis
- Pyelonephritis, including necrotizing papillitis
In diffuse proliferative lupus nephritis what will be seen with immunofluorescence?
Mesangial and capillary wall (SUBendothelial) IgG localization
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Out of the 6 patterns of glomerular disease seen in SLE, which is the most common?
Common signs/sx’s in these pts?
- Diffuse lupus nephritis (class IV)
- Hematuria and proteinuria.
- HTN and mild to severe renal insufficiency is also common
What is the most common cause of acute kidney injury (aka ARF)?
Acute tubular injury/Necrosis
What are the 2 most common etiologies causing Acute Tubular Injury?
- Ischemia i.e., hypotension, shock, HUS, TTP, or DIC
- Direct toxic injury to the tubules (drugs/toxins)
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How does the pattern of tubular damage in the PCT, PST, and ascending loop of henle seen in acute tubular injury differ between ischemic and toxic sources?
- Ischemic = patchy necrosis of these segments
- Toxic = continous necrosis of PCT and PST w/ patchy necrosis of ascending loop of henle
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Why are tubular epithelial cells particularly vulnerable to ischemia and toxins?
- Increased SA for reabsorption
- High rate of metabolism + O2 consumption w/ high energy requirements –> ischemia disrupts this
In ATI, what occurs to necrotic tubular epithelial cells over time?
Leads to?
Detach and sloughed into tubular lumen –> luminal obstruction by casts
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What is the histologic findings of acute kindey injury associated w/ ethylene glycol (aka anti-freeze)?
Often find what type of crystals in the tubular lumen?
- Marked ballooing and hydropic or vacuolar degeneration of PCT’s
- Calcium oxalate crystals
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What are the 3 stages of the clinical course of AKI/ARF and major electrolyte/lab findings in each stage?
Which stage is marked by an increases susceptibility to infection?
- Initiation - lasts about 36 hrs w/ slight decline in urine output + rise in BUN
- Maintenance - salt + H2O overload, rising BUN, and HYPERkalemia, metabolic acidosis, OLIGURIA
- Recovery - HYPOkalemiabecomes an issue as well asincreased susceptibility to infection
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What is the prognosis of ATI dependent on?
How likely are these pts to survive?
- Depends on magnitude and duration of injury
- With current supportive care, 95% of those who do not succumb to the precipitating cause recover!
What are the clinical hallmarks of Tubulointerstitial Nephritis that distinguish it from Glomerular diseases?
- Absence of nephritic or nephrotic syndrome
- Defects in tubular function –> defect in concentrating urine = polyuria and nocturia
- Salt wasting
- Dimished ability to excrete acids (metabolic acidosis)
Tubulointerstitial Nephritis is generally characterized by presence of what functional renal abnormality?
- Azotemia –> ↓ GFR
- Inability to concentrate urine –> polyuria and nocturia
Most common cause of clinical pyelonephritis arises from what?
Ascending infection from the bladder
Pyelonephritis is defined as inflammation affecting what anatomical features of the kidney?
- Tubules
- Interstitium
- Renal pelvis
What is the second most common cause of acute kidney injury (after pyelonephritis)?
Drug and toxin-induced tubulointerstitial nephritis
A small % of pts w/ analgesic nephropathy develop which malignancy?
Urothelial carcinoma of the renal pelvis
What are the major clinical signs/sx’s of acute drug-induced interstitial nephritis?
Onset?
- Begins about 15 days after drug exposure
- With fever, eosinophilia (transient), a rash, and renal abnormalities (i.e., hematuria, mild proteinuria, and leukocyturia)
What is one of the early and reversible results of ischemia associated w/ tubule cell injury?
- Loss of cell polarity
- Redistribution of Na-K-ATPase from basolateral to luminal surface of tubular cells
- Increase Na+ delivery to distal tubules
What is the major hemodynamic alteration leading to a reduction in GFR associated with ischemic tubule cell injury?
- Intrarenal vasoconstriction
- Results in reduced glomerular flow and ↓O2 delivery to functionally important tubules (TAL and PT)
ATI is characterized by what type of cell death and morphological findings?
- Focal tubular epithelial necrosis at multiple points of nephron
- Occlusion of tubular lumens by casts
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What are the eosiniphilic hyaline and pigmented granular casts seen with ATI composed of?
Tamm-Horsfall protein
What findings when present can help distinguish acute from chronic interstitial fibrosis?
- In acute, there will be more rapid clinical onset w/ edema
- Often w/ presence of neutrophils and eosinophils
Which 3 viruses may be responsible for UTI’s/renal infection, especially in immunocompromised pts such as those w/ transplants?
1) Polyomavirus
2) CMV
3) Adenovirus
What are 2 of the common predisposing medical conditions for Pyelonephritis?
1) Diabetes –> especially poorly controlled
2) Pregnancy
Which anatomic defect is an important predisposing factor for ascending infection leading to pyelonephritis?
- Incompetence of the vesicouretal valve
- Leads to reflux of urine from bladder –> ureter = vesicoureteral reflex
How can vesicoureteal reflux be acquired in both children and adults?
- Children –> congenital defect (most common) or acquired by bladder infection
- Adults –> may be acquired from persistent bladder atony due to spinal cord inury
How can vesicoureteral reflux by diagnosed?
Voiding cystourethrogram
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Although ascending infection is the most common route of bacteria entering the kidney, they may also do so hematogenously, which is most often occurs in what clinical setting?
Ongoing sepsis
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What are the morphological hallmarks of Acute Pyelonephritis?
- Patchy interstitial suppurative inflammation
- Intratubular aggregates of neutrophils
- Neutrophilic tubulitis and tubular necrosis
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Acute pyelonephritis usually shows sparing of the glomeruli, but infection by what often destroys glomeruli?
Fungal pyelonephritis (i.e., Candida) –> granulomatous interstitial inflammation
Papillary necrosis is a complication of acute pyelonephritis most often seen in which 4 patients/settings?
1) Diabetics
2) Analgesic Nephropathy
3) Urinary tract obstruction
4) Sickle Cell Disease
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Is papillar necrosis usually unilateral or bilateral and what type of morphological damage is seen?
- Typically bilateral but can be unilateral
- Tips/distal 2/3’s of pyramids have areas of gray-white to yellow necrosis (ischemic coagulative necrosis)
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What is the M:F ratio for papillary necrosis associated with diabetes mellitus?
Time course?
How do the papillae appear and are they calcified?
- Females 3:1
- Time course = 10 yrs
- Pale grayish necrosis limited to papillae; calcifications = rare
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What is the M:F ratio for papillary necrosis associated with Analgesic Nephropathy?
Time course of abuse?
How does the necrosis appear on the papillae, how diffuse is the necrosis and is there calcification?
- Females 5:1
- Time course = 7 years of abuse
- Almost ALL papillae in DIFFERENT stages red-brown necrosis w/ sloughing into calyces; calcifications are frequent
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