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Questions and Answers
Which factor primarily contributes to the risk of pyelonephritis through bladder to kidney spread?
What role does vesicoureteral reflux play in kidney infections?
Which symptom is indicative of renal involvement in establishing a diagnosis of kidney infections?
What is a common complication associated with urinary obstruction and diabetes mellitus in kidney infections?
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What characteristic finding is associated with polyomavirus nephropathy?
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What is the most common cause of acute kidney injury?
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Which characteristic is NOT associated with the 'tram-track appearance' in pathology?
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What factor is primarily responsible for decreased glomerular filtration rate (GFR) in acute tubular injury?
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Which of the following describes the pathogenesis of tubular injury in acute tubular injury/necrosis?
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In the context of acute tubular injury, which agent is least likely to cause nephrotoxic acute tubular injury?
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What determines the reversibility of acute tubular injury?
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Which feature is common to both nephritic and nephrotic syndromes when severe?
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What role do leukocytes play in the pathogenesis of acute tubular injury?
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What characterizes the Maintenance Phase of acute tubular injury?
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Which bacteria are commonly responsible for urinary tract infections that lead to acute tubular injury?
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In chronic tubulointerstitial nephritis, what type of leukocyte infiltration is typically observed?
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What is a common complication associated with the Recovery Phase of acute tubular injury?
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Which factor can lead to chronic pyelonephritis?
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What is the primary route for the ascending infection in UTIs?
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Which of the following statements about acute tubular injury is correct?
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What are common systemic effects of tubulointerstitial nephritis?
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Study Notes
Membranoproliferative Glomerulonephritis (MPGN)
- Type 3 MPGN is characterized by subendothelial, intramembranous, and subepithelial deposits seen on electron microscopy (EM).
- Clinically, it presents with nephritic syndrome, which can progress to nephrotic syndrome if severe, with concomitant nephrotic-range proteinuria.
- Light microscopy (LM) shows mesangial ingrowth, leading to glomerular basement membrane (GBM) thickening and splitting, creating a "tram-track" appearance.
- A hallmark of MPGN is the duplication of the GBM.
Acute Tubular Injury/Necrosis (ATI)
- ATI is defined as acute renal failure with evidence of tubular injury, often in the form of tubular epithelial cell necrosis.
- The term "injury" is preferred, as it is not always necrotic.
- ATI is the most common cause of acute kidney injury.
- It is typically a reversible process.
Causes of ATI
- Ischemic ATI Pattern: Caused by inadequate blood flow to the kidneys, leading to ischemia. Can be due to hypotension and shock.
- Nephrotoxic ATI Pattern: Direct toxic injury to tubules by endogenous or exogenous agents. A wide range of toxic agents can cause this.
- Mixed Patterns: Combinations of ischemic and nephrotoxic factors.
Pathogenesis of ATI
-
Tubular Injury:
- Proximal tubules are most sensitive to injury due to their toxin-concentrating abilities and high energy demands.
- Early reversible changes include loss of polarity due to redistribution of transport proteins.
- Tubuloglomerular feedback, triggered by increased sodium delivery to distal tubules, results in lower glomerular filtration rate (GFR).
- Leukocyte recruitment and inflammation worsen the injury.
- Later changes include cell detachment and luminal obstruction, increasing intratubular pressure and further reducing GFR.
- Leaking of tubular filtrate into the interstitium due to damaged endothelial cells increases interstitial pressure, further damaging tubules and decreasing GFR.
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Persistent and Severe Blood Flow Disturbances:
- Intrarenal vasoconstriction further reduces GFR, leading to decreased blood flow and oxygen delivery.
- Production of endothelin increases, while nitric oxide and prostacyclin (prostaglandin 12) production decreases.
Reversibility of ATI
- The patchy nature of damage allows non-damaged segments to repair and maintain renal function once the disturbance is removed.
- Proliferation and differentiation of epithelial cells (re-epithelialization) contribute to reversibility.
Clinical Features of ATI
- Initiation Phase (up to 36 hours): Slight decline in urine output and increase in blood urea nitrogen (BUN); oliguria (reduced urine output) due to decreased blood flow and declining GFR.
- Maintenance Phase: Sustained decrease in urine output, salt and water overload, rising BUN concentrations, hyperkalemia, metabolic acidosis. This is a reversible stage.
- Recovery Phase: Steady increase in urine output; large amounts of water, sodium, and potassium are lost due to damaged tubules. Hypokalemia (low potassium) arises, leading to increased risk of infection. Creatinine and BUN levels return to normal. Subtle, persistent functional impairment may occur for months, but eventually, complete recovery occurs.
Tubulointerstitial Nephritis
- A group of renal diseases involving inflammation of the tubules and interstitium, often with an insidious onset.
- Acute: Rapid clinical onset with interstitial edema, leukocytic infiltration, and tubular injury.
- Chronic: Predominant mononuclear leukocyte infiltration, interstitial fibrosis, and widespread tubular atrophy.
Causes of Tubulointerstitial Nephritis
- Focus on pyelonephritis and toxin-induced tubulointerstitial nephritis.
Pyelonephritis
- One of the most common kidney diseases, defined as inflammation of the tubules, interstitium, and renal pelvis.
- Acute: Typically caused by bacterial infection (UTI).
- Chronic: Results from recurrent infections, often associated with vesicoureteral reflux and obstruction.
- Affects the bladder (cystitis) and kidney and collecting ducts (pyelonephritis).
- Lower UTIs can remain localized to the bladder or spread to the kidneys.
Pathogenesis of Pyelonephritis
- More than 85% of UTIs are caused by gram-negative bacilli (normal intestinal flora).
- Escherichia coli is the most common causative agent, followed by Proteus, Klebsiella, and Enterobacter.
- Streptococcus faecalis and other bacteria, fungi, and viruses can also cause UTIs.
- Viral causes (Polyomavirus, cytomegalovirus, adenovirus) are more common in kidney allografts and immunocompromised individuals.
Routes of Infection
-
Ascending infection:
- Colonization of the distal urethra (usually in females) by coliform bacteria.
- Spread from the urethra to the bladder. Catheterization is a common cause.
- Bladder to kidney spread is influenced by:
- Urinary tract obstruction and urine stasis.
- Vesicoureteral reflux (VUR): Impaired valve allows urine to flow back, facilitating progression to pyelonephritis. VUR can be congenital, exacerbated by bacterial infection, or promoted by spinal cord injuries.
- Intrarenal reflux: Open ducts at the tips of the papillae.
Clinical Features of Pyelonephritis
- Risk Factors:
- Urinary tract obstruction
- Instrumentation
- Vesicoureteral reflux
- Pregnancy
- Gender and age
- Preexisting renal lesions
- Diabetes
- Immunosuppression and immunodeficiency
Clinical Presentation
- Sudden onset of pain at the costovertebral angle.
- Systemic signs of infection, such as fever and malaise.
- Urinary tract irritation (dysuria, frequency, urgency).
- Pyuria (increased leukocytes in urine), which is not specific to kidney involvement.
- Renal casts indicate renal involvement as they form within tubules.
- Diagnosis confirmed by quantitative urine culture.
- Antibiotic treatment typically resolves symptoms; however, recurrent infections are possible.
Viral Pyelonephritis (Polyomavirus Nephropathy):
- Nuclear enlargement and intranuclear inclusions visible under the light microscope
- Interstitial inflammatory response
- Treatment: Reduction in immunosuppression
Complications of Pyelonephritis:
- More serious manifestations and increased risk of recurrent infections in patients with urinary obstruction, diabetes mellitus, or immunodeficiency.
- Papillary necrosis can lead to acute renal failure.
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Description
This quiz covers key aspects of Membranoproliferative Glomerulonephritis (MPGN) and Acute Tubular Injury/Necrosis (ATI). It examines the characteristics, clinical presentations, and causes of these renal conditions. Test your understanding of the pathophysiology and microscopy findings associated with MPGN and ATI.
