Renal Flashcards
Removal of substances from blood into renal tubule at glomerulus.
Filtration
Removal of substances from blood into renal tubule at peritubular capillaries.
Secretion
Return of substances from renal tubule into blood at peritubular capillaries.
Reabsorption
Removal of substances from renal tubule through urine.
Excretion
Nephrons contain these parts:
- Renal corpuscle (glomerulus and Bowman’s capsule)
- Proximal convoluted tubule
- Loop of henle
- Distal convoluted tubule
- Collecting tubules
This part of the nephron actively transports sodium along with glucose, amino acids, etc. Water follows by solute drag. Counter transport of H+ and Na+. Almost all reabsorption occurs here but none of it is under hormonal regulation.
Proximal convoluted tubule
This part of the nephron reabsorbs sodium and potassium along with some water and generates interstitial salt gradient.
Loop of henle
This part of the nephron does the reabsorption of sodium, potassium reabsorption and secretion, hydrogen ion secretion, and is the site of aldosterone action.
Distal convoluted tubules
Water is reabsorbed here and it requires the interstitial salt gradient produced by the loop of henle. Site of ADH action.
Collecting tubules
The volume filtered from the glomeruli into Bowman’s space per unit of time.
Glomerular filtration rate
GFR is around this per day:
180 liters per day
This is an index of functioning renal mass.
Total GFR
The major driving force for filtration.
Hydrostatic pressure
The forces opposing filtration.
Osmotic pressure
Urine formed by these 3 processes:
- Glomerular filtration
- Tubular reabsorption
- Tubular secretion
This system helps regulate blood pressure and maintain blood volumes.
Renin-angiotensin system
Is released from the posterior pituitary and acts on renal tubules to allow for water reabsorption that depends upon the formation of a salt gradient by the loop of henle.
ADH
This hormone is released from cells of the cardiac atria in response to increased stretch and work to: counter fluid conserving effects to reduce blood volume and relieve blood pressure.
Atrial natriuretic peptide ( ANP)
ANP works generally opposite of
Aldosterone
The process of emptying the bladder.
Micturation
Specific gravity of urine should be:
1.003 to 1.030
A measure of urea in the blood
BUN
This reflects GFR and functional capacity of kidneys.
Serum creatinine
Provides an assessment of renal function.
GFR
Agents that increase water excretion.
Diuretics
Act at the proximal tubule to shift the osmotic balance. Ex mannitol
Osmotic diuretic
These work by inhibiting transports in the loop of Henle. This destroys the salt gradient generated by the loop of Henle and prevents water reabsorption under the influence of ADH from the collecting duct. Ex Lasix
Loop diuretics
These block the Na+ Cl- symporter in the DCT to block sodium reabsorption, this water remains in the lumen of the renal tubule for excretion.
Thiazide diuretics
These inhibit aldosterone, blocks Na+ reabsorption and increased K+ retention. Ex spironolactone
Potassium sparing diuretics
Represents several pathological states and usually involves inflammation of the glomerulus. May present with hematuria or proteinuria.
Glomerularnephritis
Is characterized by the passage of both protein and red blood cells out of the urine.
Nephritic syndrome
Five categories of glomerular disease:
- Acute nephritic syndrome
- Rapidly progressive glomerulonephritis (RPGN)
- Nephrotic syndrome
- Asymptomatic hematuria or proteinuria
- Chronic glomerulonephritis
Characterized by hematuria, proteinuria, azotemia, edema, and hypertension. May occur as a primary disease or secondary to other diseases such as lupus.
Acute nephritic syndrome
Progression of renal failure over days to weeks, often in the context of nephritic syndrome. Does not have a specific cause, but involves proliferation of glomerular cells. Characterized by formation of crescents initiated by the passage of fibrin into the Bowman’s space as a consequence of increased permeability of the basement membrane.
Rapidly progressive glomerulonephritis
An autoimmune disease caused by the formation of antibodies to the basement membrane and is an example of RPGN.
Goodpasture syndrome
Not a specific disease but a constellation of findings resulting from glomerular permeability and protein loss to the urine. Characterized by massive loss of proteinuria and lipiduria.
Nephrotic syndrome
Oftentimes does not present with outward signs and symptoms. May be due to the presence of IgA immune complexes that result in glomerular inflammation.
Asymptomatic hematuria or proteinuria
A hereditary form of nephritis associated with mutations in the collagen biosynthesis pathway genes. Most commonly inherited as an x-linked autosomal dominant trait.
Alport syndrome
Characterized by persistent proteinuria with or without hematuria and slowly progresses to chronic renal failure. Characterized by irreversible and progressive glomerular and tubulointerstitial fibrosis.
Chronic glomerulonephritis
Disorders that affect interstitial space surrounding the renal tubules. May be either acute or chronic.
Tubulointerstitial disease
An infection of the kidney tissue and pelvis, usually by bacteria. Bacteria are usually gram negative and come from GI tract.
Acute pyelonephritis
Often occurs as a result of hematogenous spread of bacteria and infection via the urethra or instrumentation.
Acute pyelonephritis
May be idiopathic or associated with renal obstruction or reflux (substances that have descended down the ureter then come back up). Obstructions may be kidney stones, neurogenic or congenital such as strictures. Represents a progressive disease characterized by scarring and deformation of the renal calyces.
Chronic pyelonephritis
Most common cause of acute kidney injury characterized by a rapid decline in renal function. Typically see elevations in BUN levels and creatinine with a decline in urine output.
Acute tubular necrosis
Acute tubular necrosis is classified into these 2 categories:
- Ischemic
2. Nephrotoxic
Results from a decreased perfusion or inadequate oxygenation to the renal tubules.
Ischemic atn
Results from a number of agents that directly and specifically damage the renal tubules .
Nephrotoxic atn
Three phases of ATN:
- Initiation
- Maintenance
- Recovery
This phase of ATN is dominated by the initiating cause of ATN and azotemia. Usually lasts for several years.
Initiation phase
This phase of ATN is characterized by oliguria. Lasts for about a week. Most fatalities occur in this phase.
Maintenance
This phase of ATN is characterized by profuse diuresis with continues recovery of renal function. Full recovery may take years.
Recovery phase
2 forms of poly cystic kidney disease:
- Adult autosomal dominant form
2. Infantile autosomal recessive form
This is one of the most common life-threatening genetic diseases.
PKD
Involves the obstruction of urine flow as it exits from the kidney toward the bladder.
Obstructive disorders
Obstruction of urine outflow can also give rise to:
Hydronephrosis or dilation of the renal pelvis resulting in atrophy of kidney
Most common cause of upper urinary tract obstruction.
Renal calculi
This is released by the posterior pituitary and is released in response to either low blood pressure or increased concentration of salts.
ADH
This results in fluid overload or a dilution syndrome.
SIADH
A condition in which kidneys are unable to conserve water. Patients have polydipsia and polyurea.
Diabetes insipidus
Diabetes insipidus is caused by a lack of:
ADH
Types of diabetes insipidus:
- Central
2. Nephrogenic
Is characterized by a decrease in kidney function resulting in insufficient filtration of products from the blood.
Renal failure
This is characterized by an acute insult that produces a rapid loss of function. It is often reversible with adequate treatment.
Acute renal failure
This is the progressive deterioration of function. Is usually not reversible.
Chronic renal failure
Renal failure is determined by a decrease in this:
GFR
Indicated that the underlying cause is due to the blood supply to the kidney.
Prerenal
Indicates that the underlying cause is within the kidney itself.
Intrinsic or intrarenal
Indicates that there are problems with the urinary tract or the outflow from the kidney.
Postrenal
Is manifested by oliguria and a disproportionate elevation of BUN relative to serum creatinine levels.
Prerenal failure
Most common cause of intrinsic or intrarenal disease is:
ATN
Results from obstruction of urine outflow from the kidneys:
Postrenal diseas
The progressive loss of renal function over a period of months or years.
Chronic kidney disease
As kidney function decreases:
- Bp may increase
- Urea accumulates leading to azotemia
- Hyperkalemia
- Anemia and fatigue
- Fluid volume overload
- Elevated phosphate
- Hypocalcemia
Refers to a general condition of elevated serum levels of nitrogen containing substances in the blood including urea, creatinine, and Uric acid.
Azotemia
Refers to the clinical syndrome of renal failure with azotemia:
Uremia
The lack of bladder control due to a neurologic condition.
Neurogenic bladder
The bladder is innervated by this but under the control of this.
Autonomic nervous system
CNS
This is characterized by a failure to store urine and results from neural lesions above the level of the sacral cord.
Spastic bladder
This is characterized by failure to empty the bladder and results from neural disorders affecting the motor neurons in the sacral cord or peripheral nerves.
Flaccid bladder
Most bladder cancers are from these:
Transitional cell carcinomas
