CHAPTER 25 – DISORDERS OF RENAL FUNCTION Flashcards
Describe two types of immune mechanism involved in glomerular disorders
Type 1
-injury resulting from antibodies reacting with fixed glomerular antigens or antigens planted within the glomerulus
Type 2
-injury resulting from circulating antigen-antibody complexes that become trapped in the glomerular membrane
Use the terms proliferation, sclerosis, membranous, and mesangial to explain changes in glomerular structure that occur with glomerulonephritis.
These are categorized by appearance
Proliferative
-infiltration of WBC and proliferation of glomerular cells
Sclerosis
-increased in extracellular matrix
Membranous
-thickening of glomerular capillary wall
Diffuse/focal/segmental
-EG: Mesangial, involves only mesangial cells
Compare the five classifications of glomerular syndromes.
Nephrictic Syndrom
-produces a proliferative inflammatory response, relating to a decrease in GFR, fluid retention and nitrogenous waste accumulation
Nephrotic Syndrome
-increased permeability of the glomerulus, resulting to a loss of plasma protein
Glomerular disorders effects the semipermeable properties of the glomerular capillary membrane that allow water and small particles to move from the blood into the urine filtrate, while preventing blood cells and plasma proteins from leaving the circulation
Differentiate the pathology and manifestations of the nephrotic syndrome from those of the nephritic syndrome
Acute Nephritic Syndrome
-inflammatory response occluding the glomerular capillary lumen and damaging glomerular capillary wall
Manifestations: Hematuria (hallmark sign) Decreased GFR Azotemia* (accumulation of nitrogenous waste, uric acid, BUN, creatinine) Oliguria Fluid retention -Edema -hypertension
Nephrotic Syndrome
-is the integrity of the glomerular membrane affected by medication, neoplasms, or inflammation.
it is characterized by:
- massive proteinuria
- lipiduria
- hypoalbuminemia
- edema (anasarca)
- hyperlipidemia
- increased GFR
Relate the proteinuria, hematuria, pyuria, oliguria, edema, hypertension, and azotemia that occur with glomerulonephritis to changes in glomerular structure.
??Asymptomatic Hematuria or Proteinuria
IgA nephropathy (Berger disease) IgA complex deposits d/t inflammation
Alport syndrome (hereditary) that results in hematuria
Chronic Glomerulonephritis
Acute forms either resolve or progress
Small kidneys, sclerosed glomeruli, etc.
Explain how diseases such as systemic lupus erythematosus, diabetes mellitus, and hypertension result in glomerular injury.
Systemic Lupus Erythematosus
- Most glomerular injury is triggered by the deposition of immune complexes within the glomerular wall - causing inflammation
Diabetes Mellitus
-The lesions of diabetic nephropathy most commonly involve the glomeruli and are associated with three glomerular syndromes: nonnephrotic proteinuria, nephrotic syndrome, and chronic renal failure.
- Widespread thickening of the glomerular capillary basement membrane occurs in almost all persons with diabetes and can occur without evidence of proteinuria.
- This is followed by a diffuse increase in mesangial matrix, with mild proliferation of mesangial cells. As the disease progresses, the mesangial cells impinge on the capillary lumen, reducing the surface area for glomerular filtration
Hypertension
-ere is narrowing of the arterioles and small arteries, caused by thickening and hyalinization of the vessel walls. As the vascular structures thicken and perfusion diminishes, blood flow to the nephron decreases, causing patchy tubular atrophy, interstitial fibrosis, and a variety of changes in glomerular structure and function
Explain the differences between acute and chronic pyelonephritis
Acute Pyelonephritis
Cause:
Bacterial infection of upper UT with intrarenal reflux
Contributing factors Outflow obstruction Catheterization/urinary instrumentation Vesicoureteral reflux Pregnancy Neurogenic bladder
Manifestations Rapid, chills, fever Ache/pain unilateral or bilateral Costovertebral angle Dysuria, frequency, urgency N&V, abdominal pain radiating to the back Treatment Symptomatic pain relief Fluids to aid dysuria Antibiotics
Chronic Pyelonephritis
Scarring and deformation of renal calyces and pelvis, with atrophy and thinning of cortex
Primarily affects proximal and distal tubules
Causes:
Recurrent or persistent infection, intrarenal reflux
Symptoms:
loss of tubular function and the ability to concentrate urine give rise to poly uria and nocturia and mild proteinuria
Explain the vulnerability of the kidneys to injury caused by drugs and toxins.
- because of their large blood flow and high filtration pressure, the kidneys are exposed to any substance that is in the blood
- the kidneys are also active in the metabolic transformation of drugs and therefore are exposed to a number of toxic metabolites
-drugs are toxic substances can damage the kidneys by causing a decrease in renal blood flow, obstructing urine flow, directly damaging tubulointestintial structures, or producing hypersensitivity reactions
Effect dependent on: Action of drugs/toxins Number of toxins involved Existence of pre-renal issues that decrease blood flow to kidney Formation of crystals Hypersensitivity response
Discuss the etiology, pathophysiology, and typical manifestations of autosomal dominant polycystic kidney disease.
Polycystic Kidney Disease Inherited autosomal dominant Generally older population; progresses slowly Fluid-filled cysts in kidney and liver Less-so spleen, pancreas
Deformity of epithelial cell interfere with fluid absorption/cellular maturation resulting in cyst formation
Inflammatory mediators accumulate, and renal tubular cells are destroyed
Kidneys enlarged
Manifestations Pain Hematuria Infected cysts – UTI Hypertension Complications Diverticula Nephrolithiasis (15-20% of PKD, polycystic kidney disease) Valvular deformities Cerebral artery aneurysm (10-30% of PKD patients)
List common causes of urinary tract obstruction.
Renal Pelvis
Calculi, necrosis
Ureter
Calculi, pregnancy, tumors, stricture, congenital origins
Bladder & ureter
Calculi, neurogenic bladder, cancer, benign prostatic hypertrophy and strictures
MANIFESTATION
Recurrent UTIs
Minimal to severe pain Dependent of level and degree of obstruction Complete obstruction Oliguria/anuria Renal failure
Describe the effects of urinary tract obstruction on renal structure and function.
Stasis of urine Causes UTI (common), stone formation
Progressive dilation of renal collecting ducts & tubular structures
Causes destruction & atrophy of renal tissue
Hydronephrosis
Urine-filled dilation of renal pelvis and calyces d/t obstruction of outflow, leading to atrophy of kidney
Cite three theories that are used to explain the formation of kidney stones.
- increased in blood and urinary levels of stone components and interactions among the components
- anatomic changes in urinary tract structures
- metabolic and endocrine influences
- dietary and intestinal absorption factors
- urinary tract infections
Explain the mechanisms of pain and infection that occur with kidney stones
Stagnation of urine predisposes to infection, which may spread throughout the urinary tract. When present, urinary calculi serve as foreign bodies and contribute to the infection
pain due to distention of the collecting system and renal capsule. Acute supravesical obstruction, stones are lodged in the ureter, is associated with excruciatingly severe pain.
By contrast, more insidious causes of obstruction, such as narrowing of the ureteropelvic junction, may produce little pain but cause total destruction of the kidney.
Renal colic is colicky pain that accompanies stretching of the collecting system or ureter.
The symptoms of renal colic are caused by stones 1 to 5 mm in diameter that can move into the ureter and obstruct flow.
Classic ureteral colic is manifested by acute, intermittent, and excruciating pain in the flank and upper outer quadrant of the abdomen on the affected side. The pain may radiate to the lower abdominal quadrant, bladder area, perineum, or scrotum in the man.
Non- colicky pain is caused by stones that produce distention of the renal calyces or renal pelvis. The pain usually is a dull, deep ache in the flank or back that can vary in intensity from mild to severe. The pain is often exagger- ated by drinking large amounts of fluid.
Describe methods used in the diagnosis and treatment of kidney stones.
- urinalysis, plain film radiography, intravenous pyelography, and abdominal ultrasonography.
- Urinalysis provides information related to hematuria, infection, presence of stone-forming crystals, and urine pH.
- Most stones are radiopaque and readily visible on a plain radiograph of the abdomen.
- The noncontrast spiral CT scan is the imaging modality of choice in persons with acute renal colic.
- Intravenous pyelography (IVP) uses an intravenously injected contrast medium that is filtered in the glomeruli to visualize the collecting system of the kidneys and ureters.
- Abdominal ultrasonography is highly sensitive to hydronephrosis, which may be a manifestation of ureteral obstruction.
- A new imaging technique called nuclear scintigraphy uses bisphosphonate markers as a means of imaging stones. This method has been credited with identifying stones that are too small to be detected by other methods.
Treatment: Analgesics, Anti-spasmotics Allopurinol Changes pH to decrease acidity Increased fluids to produce 2 liter/day Strain urine Diet modification Extrancoporeal shockwave lithotripsy (ESWL) Ureteroscopic removal Percutaneous nephrolithotomy
Characterize Wilms tumor in terms of age of onset, possible oncogenic origin, manifestations, and treatment.
Wilms Tumor (nephroblastoma)
Most common malignant abdominal tumor in children (ages 3-5)
Usually encapsulated
Associated with other congenital anomalies
Symptoms: abdominal mass, hypertension, abdominal pain, vomiting
Treatment involves surgery, chemotherapy, and sometimes radiation therapy.
