Week6: Chapter 13: The urinary tract Flashcards
The formation of urine is accomplished in the
nephron- basic funcional unit of each kidney
Secretory functions of the kidney
Secretes renin
secretes erythropoietin
Diagram of the kidney

Facts for understanding the kidney:
primary function
- ) Primary funtion of the kidney is to excrete urine.
- The kidneys must be anatomically normal
- body must have sufficient blood flow and adequate hydration
- hormones also regulate renal function: antidiuretic hormone (ADH) from the posterior pituitary, and atrial natriuretic hormone from the atria of the heart, Aldosterone from adrenal cortex
- passages must be patent to excrete urine
Renal failure classifications
- pre-renal: shock
- Renal: kidney diseases
- post-renal: obstruction
Facts to know about the kideny:
-infection
The urinary tract is extremely sensitive to bacterial infections.
The kidneys are perfused constantly by a high volume of blood, which is filtered in the glomeruli.
Bacteria found in the circulation thus have a good chance of entering and colonizing the kidneys and causing a urinary tract infection (UTI).
Moreover, because the ure-thral opening lies external to the body, bacteria may easily enter the urinary tract through it as well.
UTIs that are acquired from bacteremia are called descendingor hematogenous infections, whereas those attributable to upstream bacterial spread are called ascending infections
Facts to know about the kidney:
Glomeruli and infection
The specialized capillaries of the glomeruli are a ready target for bloodborne antibodies.
The glomeruli filter large amounts of blood.
During this process, their basement membranes are exposed to potentially noxious plasma components—most notably, antibodies and antigen-antibody complexes.
Glomeruli are thus often involved in many systemic autoimmune diseases mediated by antibodies. Antibody-mediated disease of the glom-eruli is known as glomerulonephritis and may be acute or chronic”
Facts to know about the kidney:
Renal tubules
Renal tubules are composed of highly specialized cells that are very sensitive to a lack of oxygen and to the adverse action of toxins.
Because the proximal tubular cells have the most complex function of all parts of the nephron, and require the most oxygen, they are most suscep-tible to hypoxia or anoxia.
Even a short interruption of blood supply or a hypoperfusion of the kidneys, as typically occurs in shock or heart failure, results in tubular necrosis.
Many drugs, poisons, heavy metals, and endogenous waste products that are filtered through the glomeruli are taken up by the proximal tubular cells and may adversely affect them.
For example, mercury salts inactivate the enzymes of the proximal tubules and, if ingested in large amounts (e.g., in suicidal mercury poisoning), can cause necrosis of the proximal tubules.”
Facts to know about the kideny: carcinogens
The urinary tract is exposed to many carcinogens that are excreted in urine
ex. bladder cancer r/t carginogens of tobacco smoke excreted in urine
Facts to know about the kidney: presentation of diseases
May present with local or systemic symtpoms
-a variety of symptoms that may be either localized to the urinary tract or systemic, affecting the entire body.
The best-known local symptom is the flank pain that occurs with kidney infection (pyelonephritis) or renal tumors.
Painful urination (dysuria) is the best-known symptom of cystitis.
Urinary colic is a symptom associ-ated with urinary stones impacted in the ureters.
Colic attacks of spasmodic pain occur as the ureteral smooth muscles contract in an effort to propel the stone and relieve the urinary obstruction”
Polyuria, oliguria, anuria
polyuria: overproduction of urine
oliguria: low urine output
anuria: no urine output
pyuria: pus in urine (leukocytes, appears turbid)
Bacteremia: numerious bacteria in urine
What is uremia?
Characterized by
“poisoning with urine”
Characterized by retention of water; minerals (e.g., sodium, potassium, chloride, calcium, and phosphate); organic substances, such as creatinine or uric acid; and other nitrogen-rich substances, such as ammonia, measured in the clinical laboratory as blood urea nitrogen (BUN).
Hypercalcemia or hyperkalemia endanger life, because these metabolic changes may cause cardiac arrest
Chronic uremia?
Marked by
Chronic uremia is marked by profound neurologic changes and depression of the central nervous system, which initially presents as somnolence and fatigue and ultimately results in coma and death.
Fortunately, by an act of Con-gress introduced in the 1970s, all Americans are entitled to free treatment of chronic renal failure; therefore, end stage chronic renal disease (uremia) is a rare cause of death in the US. Clinically, renal failure is encountered usually only in patients who have many other severe diseases or suffer from decompensated untreatable multiple organ failure.”
Polycystic kidney disease
- autosomal dominant
- r/t mutatin for gene coding polycystin-1, a cell-to-cell adhesion molecule that holds cells together
- cysts, increase weight 20x normal, 3000-4000g
cysts are from obstructed tutbules and contain fluid
resons for obstruction is unknown, but renal function is gradually impaired.
renal failure by 40-50 yo
Glomurulopathies: table

Catagories of glomerulopathys
Immunologic: glomerulonephritis
Metabolic: diabetes, amyloidosis
Circulatory: HTN, atherosclerosis, disseminated intravascular coagulation
Glomerular Disease: Immunologic
immunologic injury is most often mediated by antibodies and can be classified as a type II (cytotoxic) or type III (immune complex) hypersensitivity reaction.
Pathologic studies reveal that such injury is marked by deposits of immunoglobulins in the glomeruli.
If the deposition of immunoglobulins on GBM evokes an inflammatory reaction, the disease is classified as glomerulonephritis.
Those glomerulopathies that have an immunologic patho-genesis or a presumptive immunologic pathogenesis but that do not show signs of inflammation carry names without the suffix -itis (which is reserved for inflammatory disease). Within this category, the most important diseases are lipoid nephrosis, membranous nephropathy, and immunoglobulin A (IgA) nephropathy.
Immune-mediated glomerulonephritis can occur in an isolated form (primary) or in the course of a systemic disease (secondary), as in systemic lupus erythematosus (SLE) or granulo-matosis with polyangiitis. Primary glomerulonephritis is often limited to the glomeruli, whereas secondary glomerulone-phritis is usually associated with tubulointerstitial renal inflammation.”
metabolic glomerular disorders
best example is DM
Diabetes causes biochemical changes in the composition of the GBMs, which become thickened and “leaky” as a result of a loss in their selective semiperme-ability.
Diabetic glomerulosclerosis, like other metabolic glomerulopathies, is also associated with pathologic changes involving other parts of the kidney, including arterioles, renal tubules, and interstitial spaces”
Cirulatory disturbances of the glomeruli
- Atherosclerosis of the renal arteries is typically associated with hypoperfusion, which leads to involution and hyalin-ization of glomeruli.
- The sudden onset of hypertension may cause fibrinoid necrosis of the glomerular capillaries.
Shock is often associated with disseminated intravascular coagula-tion (DIC) and the formation of microthrombi in the glo-merular capillaries.
Syndromes of glomerular diseases
Rapidly progressive glomerulonephritis: is characterized by a loss of renal excretory function over a period of several weeks. The destruction of glomeruli presents initially with hematuria, progressing fast to oliguria, and finally to anuria. Acute renal failure is typically caused by crescentic glomerulonephritis.
- Nephritic syndrome: is diagnosed on the basis of typical clinical and laboratory findings. These include generalized edema, hypertension, hematuria, protein-uria, and hypoalbuminemia. Acute nephritis syn-drome is usually caused by acute poststreptococcal or postinfectious glomerulonephritis. The most common cause of chronic nephritic syndrome is systemic lupus erythematosus.
- Nephrotic syndrome is characterized by general-ized edema, proteinuria, hypoalbuminemia, and often hyperlipidemia and lipiduria. The most common causes of nephrotic syndrome in adults are focal glo-merulosclerosis, membranous nephropathy, and diabetes. Lipoid nephrosis is the most common cause of nephrotic syn-drome in children.
- Isolated glomerular hematuria, with or without proteinuria, is usually not accompanied by constant clinical symptoms and generally can be diagnosed only on the basis of abnormal urinary findings. This syndrome, as typically seen in IgA nephropathy (Berger’s disease), may progress to chronic renal failure like any other immune-mediated glomerulonephritis.”
Acute Glomerular Nephritis: diagram

Acute Glomerulonephritis:
- immune mediated glomerulopathy that occurs 2 weeks after an infection (strep upper resp)
- the anigen/antibody complexes get stuck in basement membrane and activate complement, and attract inflammatory cells in to the kidney
- these cells occlude the capillaries, preventing blood flow through the glomerulus
Acute Glomerulonephritis: Clinical features
presents with nephritic syndrome
The GBMs damaged by inflammation become permeable to proteins and even allow the passage of RBCs into the primary filtrate, which accounts for the proteinuria and hematuria.
Reduced glomerular blood flow through the inflamed glomeruli results in a reduced glomerular filtration rate and consequently reduced urinary output (oliguria).
The urine of these patients typically appears murky brown, resembling “bouillon soup,” a color resulting from the entry of broken RBCs into the urine.
Loss of proteins, mostly albumin, in the urine causes hypoalbuminemia, which, together with retention of sodium, results in edema.
This edema is thus in part as a result of the loss of oncotic pres-sure of the plasma, secondary to a loss of albumin in urine, and is also in part as a result of the increased volume of extracellular fluids from the sodium retention in oliguria.
Edema is most pronounced on the face, and especially in the loose subcutaneous tissue around the eyes. Edema of the brain and hypertension typically cause headaches and somnolence. The hypertension is caused by reduced blood flow through the arterioles leading to the inflamed glom-eruli, which elicits a release of renin from the juxtaglomeru-lar apparatus in the afferent arteriole.
inflammation short lived, recover completely. 1-2% have renal fail
Crescentic Glomerulonephritis
- term to describe severe glomerular injury, accompanied by formation of exudate in the glomerular urinary space
- the exudate is macrophages that have crossed through the damaged glomerular capillaries into the urinary space between the capillary tufts and Bowman’s capsule
The term derives from the fact tha the inflammatory cells surround the compressed capillary loops in the form of a crescent moon.
Macrophages are gradually replaced by fibroblasts, which secrete collagen, leading to the scarring and complete obliteration of glomeruli.
Crescentic glomerulonephritis usually occurs after focal necrosis and rupture of GBMs.
Such focal necrotizing glomerulonephritis is typically found in Goodpasture’s syndrome, an autoimmune disease characterized by the formation of antibodies to the body’s own basement mem-brane component—collagen type IV. Injury of collagen type IV in the lungs causes intraalveolar hemorrhage. In the glomeruli the antibodies cause rupture of basement membrane.
In the glomeruli the antibodies cause rupture of the basement membranes.
Macrophages exit through the holes in the GBMs and accumulate in the urinary space, forming the crescents that compress the capillary loops.
Because no blood flows through the compressed capillary loops, glo-merular filtration ceases and anuria (i.e., acute renal failure) ensues. Clinically the disease is known as rapidly pro-gressive glomerulonephritis (RPGN). Most patients never recover, and their survival depends on continuous dialysis or kidney transplantation”
Membranous nephropathy
Immune-mediated glomerulopathy characterized by diffuse (“membranous”) thickening of the GBMs secondary to massive formation of immune complexes along the epithelial (urinary) side of the GBMs.
In contrast to acute glomerulonephritis, which causes nephritic syndrome, membranous nephropathy pres-ents as a typical nephrotic syndrome. There is no evidence of inflammation, the glomeruli do not contain any inflam-matory cells, and the urine is devoid of RBCs and inflam-matory cells”
most common immune nephrotic syndome in adults
does not respond to steroids
protein uria, 40% disease progresses
Nephrotic syndome: as seen on microscope

what is the glomerulus
tuft of capillaries with basement membrane and epithelial cells
basement membrane
3 layers
filters particles
What you need to know about glomerular diseases
- circulating immune complexes - produce injury to epithelial cells -deposits- antigen in the basement membrane
- or antibody/antigen reaction-antibodies to antigens that exist in the basement membrane

Nephrotic syndrome
- proteinuria >3.5
- hypoalbuminemia <3
- peripheral edema
- hypercholesterolemia
Nephrotic Syndrome Differential
Primary: Renal
- Minimal Change: lipoidnephrosis
- Focal segmental: glomerular nephritis
- Membranous: glomeropathy?
Secondary: systemic
- amyloid
- diabetes
Lipoid Nephrosis
(mininal change disease)
Most common form of nephrotic syndrome in children. Tx. with steroids
M>F
20% adults, M=F, biopsy before tx., prognisis not as great
Pathogenesis: unknown, but could be allergen.
-May be T-cell dysfunction causing lymphokyne
causing epithelial cell damage, loss of change and size of selection, causing albinuria
- SELECTIVE loss of low weight proteins
- exaserbations and remissions
- glomeruli show no change on microscopy, can only see fusion of foot processes
Focal Segmental Glomerulosclerosis
- 5-10% of nephrotic children
- Up to 35% of nephrotic adults
- Most common cause of NS in adults
- Heavy NON-selective proteinuria
- may be idiopathic, drug induced, or inherited
- may be associated with obesity or a variety of systemic diseases
Clinical: Heavy, non-selective proteinuria
May have microscopic hematura, reduced GFR, and HTN
- on microscopy, C3 & IGM seen in sclerotic areas, and collapse of glomerulus
- most progress to renal failure slowly, a few respond to steroids
- will recur in transplanted kidneys
Membranous Nephropathy
causes
- Common cause of nephrotic syndrome in adults (peak 35-40)
- Most are idiopathic (85%), others associated with systemic diseases, toxins, drugs, infectious diseases, and metabolic abnormalities
1. Idiopathic: antibodies to antigens present on podocytes - antigens trapped in subepithelial space
- antigens to proximal tubule epithelium
2. Cirulating Immune Complexes
Membranous Nephropathy:
clinical
- nephrotic syndrome and proteinuria
- widely variable outcome, with 50% progressing to renal failure in 2-20 years
025-30% go into remission
-renal vein thrombosis can cause sudden loss of funtion in 25-50% of cases
on microscopy: uniform diffuse thickening of GBM, spike pattern
diabetic glomerulosclerosis
- occurs in 30-40% of IDDM, and 20-30% of NIDDM
- most common cause of end stage renal in USA
Pathogenesis:
glycosilation of basement membrane, hemodynamic factors, systemic and microvascular HTN
- nodules: mesangial or Kimmelsteil-Wilson (dx.)
- diffuse: uniform thickening of GBM, diffuse messangial sclerosis, diffuse mesangial proliferation (increased cellularity)
Renal Amyloid

Glomerular Nephritis

Pathogensis of Glomerular Nephritis
- Damage to GBM
- Fibrin in the Bowmans space
- fibrin, macrophages, and parietal cell proliferation for crescent

Lupus and renal disease
- 60-70% will have renal disease
- chronic proliferative glomerular nephritis: responds well to steroids
End Stage Glomerular Nephropathy
- most, if not all, can progress to end stage kidney disease
- kidneys appear shrunken and granular
Most prevalent metabolic disease affecting the kidneys
diabetes, 5-10% have renal problems
Diabetic Nephropathy
-diffuse glomerularsclerosis: thickening of basement membrane and increased amount of messengial matrix
Nodular glomerularsclerosis: increased messengial matrix leads to formation of nodules
-basement membrane of altered glomeruli show increased permeability and results in proteinuria
Vascular changes show in arterioles with hyanylosis characterized by thickening of vessel wasll and narrowing of lumen. this leads to ischemia and tubular atrophy. Papilary necrosis
Kidneys in DM are prone to pyelonephritis
Urolithiasis
-common, 5% of people will develop in at some point
Calcium (most common), struvite (complication of UTI), uric acid, cystine
- Most often found in renal pelvis or urinary bladder
- more common in men, in 20-30s
- stones in bladder tend to occur in older patients, and associated with infection
- symptoms: hematuria, renal colic
Urinary Tract Infections
- most common human diseases
- gram negative bacteria (Ecoli, Klebsiella, pseudamonas)
- Pylonephritis (kidney)
- Cystitis (bladder)
- more common in women
- pregnancy predisposes
Hematogenic and ascending infection
Hematogenic: preceedid by septicemia as a secondary infection
Ascending: (more common) catheters, intercourse
Acute Pylonephritis
suppurative infection of the kidneys
in severe infections may permeate entire kidney and renal pelvis
Chronic pylonephritis
May evolve from acute pyelone-phritis,
Persistent infection leads to destruction of the renal parenchyma and broad parenchymal scar formation. Ultimately, because of the loss of renal tissue, the affected kidney becomes small and irregularly scarred.
Because the bacteria do not grow at the same rate in both kidneys and the infection is often unilateral, kidneys affected by chronic pyelonephritis are typically asymmetric. Indeed, it is not uncommon for one kidney to be completely shrunken and the other one to be spared
Acute Cystitis:
characterized by
Acute cystitis is characterized by grossly visible congestion and mucosal hemorrhages
These changes are best visualized with cys-toscopy, a procedure in which the urologist observes the inside of the bladder with an instrument that has been introduced through the urethra. In severe cases the mucosa may be covered with pus or be ulcerated”
Chronic Cystitis
the appearance of the mucosa varies considerably and includes foci of hemor-rhage, ulceration, or thickening.
The wall of the bladder is often thick, especially if there is obstruction
Acute tubular necrosis
sudden decrease in arterial pressure resulting in hypoperfusion of the kidneys (MI, hypotensive shock).
- cortical tubules, especially proximal convoluted tubules most affected
- severe: entire cortex may become necrotic
Nephroangiosclerosis
- atherosclerosis of aorta narrowing blood flow to kidneys, leads to ischemic glomerular sclerosis and loss of glomeruli and accompanied by tubular atrophy
- kidneys are shrunken and show scarring