Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
243 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
What are two techniques for obtaining a renal sample?
|
Percutaneous route
Needle biopsy |
|
|
|
How is a renal biopsy examined?
|
Light microscopy
Immunohistochemistry Immunofluorescence Electron microscopy |
|
|
|
What are the three main compartments in the kidney?
|
Glomeruli G
Tubules T Interstitium and Blood Vessels I/BV |
|
|
|
What normal components of the normal human glomerulus are visible with light microscopy?
|
Mesangial cells
Endothelial cells Podocytes Proximal Tubules Macula densa Visceral and Parietal epithelium Capsular space |
|
|
|
What are the three different stains used on kidney samples for immunohistochemical analysis?
|
Silver stain - accentuates collagenous structures GBM: the glomerulus, mesangial matrix, glomerular basement membrane
The PAS stain - accentuates matrix and basement membrane constituents The Trichrome stain - demonstrates immune deposits as fuchsinophilic (red) structures |
|
|
|
What are the two types of immunofluorescence for renal samples?
|
Linear
Granular |
|
|
|
What are the uses of immunofluorescence regarding renal samples?
|
To identify...
The presence of immune complexes or antibodies The nature of immune complexes and antibodies The presence of complement |
|
|
|
Why is electron microscopy used to analyze renal samples?
|
It is used to identify subendothelial and subepithelial immune deposits
Reveals foot processes, nuclei of visceral epithelial cells, basement membrane, nuclei of endothelial cells |
|
|
|
What are the four patterns of glomerular lesions?
|
Focal - you see the lesion in less than 50% of the glomeruli
Diffuse - you see the lesion in all glomeruli Segmental - only a portion of an individual glomerular tuft is affected Global - involve the entire glomerulus |
|
|
|
What are the four basic tissue reactions found in glomerular diseases?
|
Proliferative or hypercellular
Basement membrane thickening Hyalinization Sclerosis |
|
|
|
Describe a proliferative, hypercellular lesion in the kidneys.
|
An increase in glomerular cell number - may include...
Leukocytes Resident glomerular cells (endothelial cells, epithelial cells (parietal cells forming crescents), mesangial cells Increase in basement membrane material (membranoproliferative) - increase in synthesis of proteins. |
|
|
|
Describe basement membrane thickening lesion in the kidneys.
|
Thickening of the capillary wall - because of immune complex deposition or increased ECM synthesis.
Best identified by PAS staining. |
|
|
|
Describe a kidney lesion with hyalinization.
|
Extracellular deposition of any material that is homogenous and eosinophilic
Usually the deposited material is made of plasma protein |
|
|
|
Describe a kidney lesion with sclerosis.
|
When collagen is in excess and leads to obliteration and hardening of the glomerulus, it is termed sclerosis
Accumulation of extracellular collagenous matrix |
|
|
|
What are the two categories for pathogenesis of glomerular injury?
|
Immunologic glomerular mechanism
Non-immunologic glomerular mechanism |
|
|
|
What are the two types of immunologic glomerular injury types?
|
Antibody-mediated injury - Ab reacts with fixed intrinsic tissue antigen, planted
Circulating immune complex deposition - exogenous, endogenous |
|
|
|
Describe antibody-mediated glomerular injury.
|
Antigen is a normal component of the GBM (collagen type IV)
Problems occur when anti-glomberular basement membrane antibodies are produced and bind to the entire length of basement membrane. May be a bacterial product (exogenous antigen) or DNA molecules (endogenous, like in SLE) Can be visualized using linear immunofluorescence. |
|
|
|
Describe circulating immune complex-deposition glomerular injury.
|
Ag/Ab complexes are trapped in the glomerulus
Highly cationic immunogens cross the GBM and deposit in the subepithelial layer Anionic complexes are excluded from the GBM and deposit in the subendothelial layer Damage occurs through complement or neutrophils - example: SLE |
|
|
|
What are some types of non-immunologic glomerular injuries?
|
Metabolic - diabetes
Hemodynamic - hypertension Deposition diseases - amyloidosis |
|
|
|
What are some clinical presentations of glomerular disease?
|
Asymptomatic urinary findings - hematuria, proteinuria
Acute nephritis Nephrotic syndrome Acute renal failure Chronic renal disease/renal failure Tubular defect UTI Nephrolithiasis |
|
|
|
With what clinical presentation is diffuse proliferative GN associated?
|
Acute nephritic syndrome
|
|
|
|
With what clinical presentation is crescentric GN associated?
|
Rapidly progressive GN, hematuria, proteinuria, renal failure
|
|
|
|
With what clinical presentation is mesangial proliferative GN associated?
|
Proteinuria
|
|
|
|
With what clinical presentation is membranoproliferative GN associated?
|
Nephritic and Nephrotic syndrome
|
|
|
|
With what clinical presentation is minimal change GN associated?
|
Nephrotic syndrome
|
|
|
|
With what clinical presentation is focal segmental GN associated?
|
Nephrotic syndrome
|
|
|
|
With what clinical presentation is membranous GN associated?
|
Nephrotic syndrome
|
|
|
|
With what structural patterns is nephrotic syndrome associated?
|
Membranoproliferative, minimal change, focal segmental, and membranous GN
|
|
|
|
With what structural patterns is proteinuria associated?
|
Mesangial proliferative GN
Crescentric GN |
|
|
|
With what structural patterns is acute nephritic syndrome associated?
|
Diffuse proliferative GN
Membranoproliferative GN (non-acute?) |
|
|
|
With what structural pattern is hematuria and rapidly progressive GN associated?
|
Crescentric GN
|
|
|
|
Which glomerular diseases present primarily with nephrotic syndrome?
|
Minimal change disease
Membranous glomerulonephritis Focal segmental glomerulosclerosis IgA nephropathy |
|
|
|
What glomerular diseases present mostly with nephritic syndrome?
|
Membranoproliferative GN
Acute post-infectious GN Crescentric glomerulonephritis |
|
|
|
What combination of S/S are associated with nephritic syndrome?
|
Macroscopic hematuria
Hypertension Periorbital oedema RBC casts in urine Mild to moderate proteinuria (<3.5gm/day) |
|
|
|
What are some possible causes for nephritic syndrome?
|
Primary glomerular disease (Poststreptococcal glomerulonephritis)
Secondary to systemic disease (glomerular involvement in SLE) Results from acute deposition of antibody in the subendothelial cell space or mesangium |
|
|
|
What are some characteristics of nephritic syndrome, hallmarks?
|
Characterized by rapid recruitment of leukocytes and platelets - inflammatory
Hallmark is increase in glomerular cell number (proliferation) Proliferating cells include - leukocyte, endothelial cells, mesangial cells |
|
|
|
What is acute proliferative GN (postinfectious)? Describe the pathophysiology, clinical presentation...
|
Occurs 1-4 weeks after Strep. infection, most frequent in children
GABHS type 12, 4, 1 in 90% of cases Low complement 90% recover Bad signs - persistent proteinuria, low GFR |
|
|
|
How does acute proliferative GN appear microscopically?
|
Uniform increase in cellularity
Diffuse (all glomeruli) - all are hypercellular Cells proliferating: endothelial, mesangial cells; PMNs Proliferative lesions present, with exudate of polymorphs |
|
|
|
What are some microscopic signs of a bad prognosis in acute proliferative GN?
|
Crescents formation
Thrombi |
|
|
|
What immunofluorescence pattern is seen in acute proliferative GN?
|
Granular pattern, large bumps
|
|
|
|
What are characteristics of an EM view of renal tissue in acute proliferative GN?
|
"humps"
Large, subepithelial deposits |
|
|
|
What is rapidly progressive GN?
|
The acute nephritic syndrome is the clinical correlate of acute glomerular inflammation.
On one end of the spectrum, it presents with Nephritic syndrome (structural pattern: proliferative GN) and on the other end, may present with RPGN (structural pattern: crescentric GN) |
|
|
|
What are some S/S of RPGN?
|
Rapidly Progressive GN
Acute renal failure Oliguria Nephritic sediment Impaired GFR Edema Hypertension Hematuria |
|
|
|
What are characteristic features of (crescentic) RPGN?
|
Rapid, progressive, severe
Severe glomerular injury >50% off glomeruli are affected Oliguria 90% of patients require long term dialysis or transplantation 3-12 month prognosis generally |
|
|
|
What are the three types of (crescentic) RPGN?
|
Type 1 - Anti-GBM
Type 2 - Immune complex mediated Type 3 - ANCA |
|
|
|
What specific clinical disease(s) are associated with Type 1 - Anti-GBM RPGN?
|
Goodpasture Syndrome
|
|
|
|
What specific clinical disease(s) are associated with Type 2 - Immune complex mediated RPGN?
|
Post infectious GN
Lupus nephritis Henoch Shonlein Purpura HSP |
|
|
|
What specific clinical disease(s) are associated with Type 3 - ANCA RPGN?
|
ANCA-associated
Wegener Granulomatosis Microscopic polyangiitis |
|
|
|
What are the gross characteristics of crescentic RPGN?
|
Kidney is large, pale, and often with petechial hemorrhage
|
|
|
|
What are the main microscopic characteristics of crescentic RPGN?
|
Crescent shaped masses of parietal proliferating parietal epithelial cells
Fibrin strands are prominent between the cellular layers of the crescent |
|
|
|
How are the typical crescent morphological formations in crescentic RPGN formed?
|
Formed by proliferation of parietal cells and migration of monocytes into Bowman's capsule.
|
|
|
|
What is nephrotic syndrome?
|
A combination of heavy proteinuria (3.5gm/day) from altered permeability of GBM and podocytes. Highly selective has proteinuria with LMW proteins, whereas poorly selective has proteinuria with HMW proteins.
Low serum albumin Hyperlipidemia Generalized pitting edema (sodium water retention) |
|
|
|
What are some markers for nephrotic range proteinuria?
|
Oval fat bodies
Red droplets of proteins and lipoproteins |
|
|
|
What are some characteristics (morphology, histology, microscopy) for nephrotic syndrome?
|
Antibody deposition in the subepithelial space
Nephrotic urinary sediment Absence of pronounced inflammatory cell infiltrate Immune complexes are shielded from inflammatory cells by GBM, hence no inflammation. |
|
|
|
What are some associated risks/sequelae of nephrotic syndrome?
|
Prone to infection
Hypercoagulopathy Microcytic Hypochromic Anemia |
|
|
|
What are the three major structural patterns associated with nephrotic syndrome?
|
Minimal change GN
Focal segmental GN Membranous GN |
|
|
|
How does nephrotic syndrome occur/present in children?
|
It occurs secondary to a primary renal disorder
Typically minimal change GN |
|
|
|
How does nephrotic syndrome occur/present in adults?
|
It occurs secondary to a systemic disease
Diabetes, amyloidosis, SLE If all secondary causes are excluded, then the most common primary cause will be focal segmental or membranous GN |
|
|
|
What is another name for minimal change GN?
|
Lipoid Nephrosis
|
|
|
|
How does minimal change GN typically present?
|
Usually a child, with proteinuria and edema
Selective proteinuria - specifically albumin No immune complexes Dramatic response to steroids |
|
|
|
What is the most common cause of nephrotic syndrome in children?
|
Minimal change GN
|
|
|
|
What are some microscopic/morphologic changes in minimal change GN?
|
Principal lesion is in visceral epithelium
Defect in charge barrier - loss of negative charge Diagnostic feature: Effacement of foot processes (visceral epithelial cells become flat), with NORMAL glomeruli in light microscopy Lipid laden cells - hence the name lipoid nephrosis. |
|
|
|
How is minimal change GN treated?
|
Completely reversible with steroid therapy
Associated with atopy (hypersensitivity type I) |
|
|
|
What is focal segment glomerulosclerosis (FSGS)?
|
Focal (less than 50% of the glomeruli)
Segmental (portion of the glomerulus) Nonselective proteinuria Poor prognosis |
|
|
|
What characterizes FSGS?
|
Poor response to steroids
Nonselective proteinuria Immunofluorescence positive Progresses to end stage renal disease Increased incidence of hematuria and hypertension (so it can progress to RPGN) |
|
|
|
Is FSGS primary or secondary renal disease? Explain.
|
Can be primary renal disease
Can be secondary, as to HIV, heroin addicts, sickle cell disease *It can occur in a transplanted kidney, so possibility of a circulating factor. |
|
|
|
What is the most common cause of nephrotic syndrome in African Americans?
|
FSGS - focal segmental glomerulosclerosis.
|
|
|
|
What are some characteristics of FSGS seen under light microscopy?
|
Hyalinosis
Sclerosis Entrapment of plasma proteins and increased ECM |
|
|
|
What is the most common primary cause of nephrotic syndrome in adults?
|
Membranous GN
|
|
|
|
How does Membranous GN typically present?
|
Patient presents with LE edema, nonselective proteinuria (albumin, globulin) - rule out systemic diseases
Few patients show spontaneous remission, few respond to steroids, most progress to end stage renal failure |
|
|
|
What are some unfavorable signs associated with Membranous GN?
|
Sclerosis
Raised BUN Hypertension |
|
|
|
What are the two general forms of Membranous GN?
|
Primary, idiopathic form - 85% of cases
Secondary form - associated with other diseases SLE, DM, pulmonary neoplasm, HBV, HCV, drugs (NSAIDs, penicillamine, gold) |
|
|
|
What are some of the histopathomorphological characteristics of Membranous GN?
|
Immune complexes localize to the subepithelial aspect of the capillary loop (between the outer aspect of the basement membrane and the podocyte)
There is uniform diffuse thickening of the basement membrane Capillary walls are thickened and numerous subepithelial spikes are present on the capillaries of this glomerulus, representing elaboration of basement membrane between subepithelial immune deposits. |
|
|
|
Describe the immunofluorescence pattern in Membranous GN.
|
There is bright granular staining of the subepithelial aspect of the capillary loops with antibody to IgG.
|
|
|
|
What disease presents with nephrotic and/or nephritic syndrome?
|
Membranoproliferative GN
There is hypercellularity - mesangium, epithelial and endothelial, basement membrane, leukocytes |
|
|
|
Describe Type I membranoproliferative GN.
|
Type 1 is immune complex mediated
Activates both alternative and classical complement pathway, serum C3 is low, IgG, C1, and C4 are deposited Subendothelial electron deposits May respond to RPGN Secondary: HBV, HCV, SLE, Schistosomiasis |
|
|
|
Describe Type II membranoproliferative GN.
|
Persistent activation of C3
Alternative pathway only is activated Low factor C3 No C1, C4 deposition No IgG deposition Dense deposits disease in GBM Primary disease of kidney |
|
|
|
What is the role of C3NeF in Type II membranoproliferative GN?
|
C3NeF is present in the serum of type II MPGN patients
C3NeF acts as Properdin in the alternative pathway for complement It stabilizes C3 convertase Ab against C3NeF will result in excessive complement activation. |
|
|
|
What is characteristic microscopically of MPGN with a silver stain?
|
There is a double contour to the basement membrane and capillary wall (splitting)
|
|
|
|
Which primary diseases of glomeruli may present with only hematuria or proteinuria, and no other clinical features?
|
IgA nephropathy
Hereditary Nephritis/Alport syndrome |
|
|
|
Describe IgA nephropathy.
|
Macroscopic recurrent hematuria concurrent with an URI or strenuous exercise, or discovered incidentally during routine examination
Asymptomatic microscopic hematuria and variable proteinuria May progress to nephrotic syndrome or RPGN |
|
|
|
What is the most common glomerulopathy worldwide?
|
IgA Nephropathy
|
|
|
|
Describe the pathophysiology of IgA nephropathy.
|
The IgA deposits localize to the mesangium, may have associated IgG and C3 deposits
There is abnormal synthesis of IgA Associated with liver disease, Crohn disease |
|
|
|
Describe hereditary nephritis/Alport syndrome.
|
Hereditary nephritis
Presents with hematuria, deafness, and eye disorders Genetic defect X-linked or autosomal dominant |
|
|
|
List the four clinical stages of renal failure.
|
Diminished renal reserve
Renal insufficiency Chronic renal failure End stage renal disease |
|
|
|
Describe diminished renal reserve.
|
GFR is 50% of normal
BUN/creatinine is normal Asymptomatic, isolated hematuria, proteinuria |
|
|
|
Describe renal insufficiency.
|
GFR is 20-50% of normal
Azotemia Anemia, hematuria, polyuria, nocturia, stress will precipitate uremia |
|
|
|
Describe chronic renal failure.
|
GFR is 20-25% of normal
Volume and solute composition normal Edema, metabolic acidosis, hyperkalemia, uremia |
|
|
|
Describe end stage renal disease.
|
GFR is <5% of normal
Uremia Symptoms very bad |
|
|
|
What are some microscopic features associated with progression of glomerular injury?
|
Glomerular sclerosis - more and more glomeruli become hard and stiff structures
Tubulointerstitial damage (disease extends to the interstitium and tubules) |
|
|
|
What types of GN may progress to chronic forms?
|
Membranous GN
Membranoproliferative GN IgA nephropathy Focal segmental glomerulosclerosis Crescentic/RPGN |
|
|
|
What are gross characteristics of chronic glomerulonephritis?
|
Small contracted kidney
Granular surface |
|
|
|
What are some microscopic characteristics of chronic glomerulonephritis?
|
Hyaline obliteration of glomeruli
Arterial and arteriolar sclerosis Atrophy and fibrosis of tubules |
|
|
|
What are clinical features of chronic GN?
|
Anemia
High BUN and Creatinine Hypertension |
|
|
|
What changes occur as chronic GN progresses to end-stage kidney disease?
|
There is irreversible loss of glomeruli
The kidney becomes end stage kidney Uremia occurs Dysfunction of all systemic organs |
|
|
|
List 5 major systemic diseases which may present with renal disorder.
|
SLE
Amyloidosis Hypertension Diabetes mellitus HIV |
|
|
|
List the five different appearances of glomerular disease in Lupus Nephritis.
|
Class 1 - normal glomeruli by LM, may or may not have deposits by EM
Class 2 - mesangial proliferation Class 3 - focal proliferative Class 4 - diffuse proliferative Class 5 - membranous proliferative |
|
|
|
With LM, typical congo red amyloid positive fibrillary deposits are found within which renal structures?
|
Glomeruli
Tubules Interstitium Blood vessels |
|
|
|
In amyloidosis, what may be seen microscopically within renal tubules?
|
Amyloid casts
|
|
|
|
Describe the pathology of renal disease in patients with Diabetes mellitus.
|
About 40% of patients with type I or II DM develop renal disease
Disease begins with microalbuminuria within a few years of DM, and progresses by 10-15 years to overt nephropathy Patient progresses to end stage renal disease within 20-25 years of onset of DM |
|
|
|
What are the effects on the blood vessels, glomeruli, tubules, and renal pelvis in diabetic nephropathy?
|
Blood vessels - afferent and efferent arteriolosclerosis, hyaline sclerosis
Glomeruli - diffuse sclerosis, nodular sclerosis (spherical accumulation of mesangial matrix known as Kimmelstiel-Wilson nodules) Tubules - atrophy and fibrosis Renal pelvis - pyelonephritis and papillary necrosis |
|
|
|
List some HIV-associated nephropathies.
|
Acute renal failure induced by drugs, shock, infection
Post-infectious GN Membranous GN associated with HBV Focal segmental glomerulosclerosis - most common form, seen in 5-10% of HIV-infected patients |
|
|
|
Describe benign nephrosclerosis in hypertension.
|
In patients with hypertension that has not progressed to malignant form
May occur in the absence of hypertension Kidney is small, has fine leathery granularity of surface. Sclerosis of renal arterioles and small arteries - hyaline arteriolosclerosis (small arteries), fibroelastic hyperplasia (reduplication of elastic tissue) Glomeruli are collapsed and tubules are atrophied Rarely causes renal failure - only decreases GFR and causes mild proteinuria |
|
|
|
What are some histological/microscopic features of benign nephrosclerosis?
|
Hyaline arteriolosclerosis
Hyperplastic arteriolosclerosis Sclerotic glomerulus Glassy thickening of arteriolar walls Fibroelastic intimal hyperplasia |
|
|
|
When would benign nephrosclerosis lead to renal insufficiency?
|
African Americans
Severe blood pressure elevation Presence of DM |
|
|
|
Describe the gross appearance of the kidney in malignant hypertension.
|
The kidney shows small petechial hemorrhages on the surface (Flea-bitten appearance)
|
|
|
|
What are the two morphologies seen in kidney lesions in malignant hypertension?
|
Fibrinoid necrosis - afferent arterioles, necrosis with no inflammatory cells, fibrin is deposited in blood vessel wall
Onion skin - interlobar vessels, smooth muscle proliferation, concentric layering of collagen (onion skin), plasma protein accumulation |
|
|
|
What is the differential for hematuria? (Hint: TICS)
|
T - trauma, toxins, tumors
I - infection, inflammation C - calculi, cysts, congenital S - surgery, sickle cell, something else |
|
|
|
What kind of trauma could cause hematuria?
|
Any injury to the urinary system, from kidney to urethra, including abdominal or back injury, prolonged exercise, foley catheter insertion
|
|
|
|
What kind of tumor could cause hematuria?
|
Renal cell cancer
Transitional cell cancer of the bladder Others: Wilm's tumor (nephroblastoma), neoplasms of the prostate and urethra |
|
|
|
What kind of toxins could cause hematuria?
|
Turpentine
Benzenes Sulfonamides Cyclophosphamide NSAIDs (acute drug-induced interstitial nephritis) |
|
|
|
What kinds of infections could cause hematuria?
|
Cystitis and polynephritis
Prostatitis Urethritis |
|
|
|
What inflammatory processes could lead to hematuria?
|
Acute and chronic nephritic syndrome (glomerulonephritis)
Interstitial nephritis Vasculitides Postirradiation Interstitial cystitis, nongonococcal urethritis |
|
|
|
Where might a person develop calculi that cause hematuria?
|
Renal, ureteral, bladder, urethra calculi
|
|
|
|
What kind of cysts cause hematuria?
|
Simple renal cysts, polycystic disease of the kidneys
|
|
|
|
What kinds of congenital anomalies may cause hematuria?
|
Hemangiomas
Arteriovenous malformation (AVM) |
|
|
|
What hematological disorders may cause hematuria?
|
Sickle Cell anemia
Hemophilia Thrombocytopenia Anticoagulants |
|
|
|
What is idiopathic hematuria?
|
A diagnosis of exclusion - made after a complete evaluation (ultrasound, cystoscopy, IVP, etc) has ruled everything else out
|
|
|
|
What are the most frequent causes of adult hematuria?
|
45% - Infection
20% - Calculi 20% - Other 15% - Cancer |
|
|
|
What could cause urine to be discolored (non-pathologic causes)?
|
Drugs: Rifampin, Sulfamethoxazole, Ibuprofen, Phenytoin, Levodopa, Nitrofurantoin, Quinine
Food: Beets |
|
|
|
What might cause a false positive for hematuria?
|
Hemaglobin can be from intravascular hemolysis
Myoglobin can also register as blood |
|
|
|
What might cause a false negative for hematuria?
|
Large amounts of ascorbic acid (vitamin C) can mask hemoglobin and RBCs
|
|
|
|
How is hematuria investigated?
|
Dipstick evaluation (not too accurate)
Microscopic evaluation of spun urine sediment (more accurate) Look for...RBCs, WBCs, bacteria, fungi |
|
|
|
Define microhematuria.
|
> 3 RBCs per high-power field in 2 out of 3 specimens
|
|
|
|
What is indicated by RBC casts? WBC casts?
|
RBC casts - glomerular bleeding
WBC casts - with bacteria, they indicate pyelonephritis |
|
|
|
What other laboratory tests may be useful in determining presence/cause of hematuria?
|
CBC
BUN Creatinine Bleeding panel: PT, PTT, hemoglobin electrophoresis, sickle cell test Urine cytology - looks for tumor cells |
|
|
|
What is the most common cause for dysuria?
|
Infection
Cystitis Prostatitis Pyelonephritis Urethritis |
|
|
|
What are some non-infection causes for dysuria?
|
Hormonal - hypoestrogenism during menopause
Malformations - benign prostatic hyperplasia, urethral strictures Neoplasms - bladder, prostate, vulva, etc. Trauma - catheter placement, "honeymoon" cystitis Psychogenic - stress disorder, major depression |
|
|
|
Which infections that cause dysuria are most common in women? In men?
|
Men: Gonorrhea, Chlamydia, non-gonococcal urethritis (nonspecific STI)
Women: UTI, other vaginal infections (STI) |
|
|
|
What is cystitis?
|
A bladder infection, most often due to Escherichia coli and other fecal bacteria, typically one's own fecal bacteria.
STIs must also be considered in sexually active patients Symptoms: Dysuria, Urinary Frequency, Hematuria. Fever etc. are rare. Women more often at risk (DUH). |
|
|
|
Is cystitis "complicated" or "uncomplicated"?
|
Uncomplicated - which means that secondary problems like urosepsis are rare
|
|
|
|
How is cystitis treated?
|
A short course of PO ABx is usually sufficient, and the patient should be instructed on proper hygiene and lifestyle modifications to avoid future infections.
Organisms: 90-95% > E. coli, S. saprophyticus Women 3-7 days of BID fluoroquinolone Men 7-10 days of BID fluoroquinolone (longer because of prostate involvement) |
|
|
|
What is pyelonephritis?
|
Kidney infection, usually unilateral, due to the same bacteria as cystitis (E. coli, S. saprophyticus).
Usually results from ascending untreated/undertreated cystitis, higher risk from pregnancy due to pressure on the bladder. |
|
|
|
Is pyelonephritis "complicated" or "uncomplicated"?
|
Complicated - secondary problems like urosepsis may occur.
Because the kidneys process blood, bacteria can enter the blood stream. Symptoms usually include unilateral flank pain, fever, malaise. |
|
|
|
What are some sequelae of pyelonephritis?
|
There may be scarring in the ureters
Recurring infections (chronic pyelonephritis) Inflammation, tissue destruction (tubulointerstitial nephritis) |
|
|
|
How is pyelonephritis treated?
|
Antibiotics usually curable - sometimes IV ABx are necessary.
Mild-moderate illness without N/V = 10-14 days Outpatient PO fluoroquinolone Severe illness or urosepsis - hospitalization, many IV alternatives: fluoroquinolones, ceftriaxone, beta-lactam ABx, etc. Subsequent PO fluoroquinolone therapy for 10-21 days, with duration depending on severity of infection and susceptibility of strain. |
|
|
|
What risk factors are associated with pyelonephritis?
|
Increased frequency of sexual intercourse
UTI within previous 12 months Diabetes Stress incontinence within previous 30 days New sex partner within the previous year Recent spermicide use UTI history in the participant's mother |
|
|
|
What is nephrolithiasis?
|
Also called calculi, or "stones" - they develop in the kidneys and can migrate through the ureters, into the bladder, and exit the body.
Migration very painful - causes tissue to stretch, causing renal colic |
|
|
|
What is the differential diagnosis associated with nephrolithiasis?
|
Pyelonephritis
Aortic dissection Appendicitis Biliary colic Acute pancreatitis Perforated ulcer Diverticulitis Gynecologic disorder Viral gastroenteritis |
|
|
|
Who is more often affected with nephrolithiasis, men or women?
|
Men - peak age of onset 20-30 years of age
|
|
|
|
How do kidney stones develop?
|
An increased urinary concentration of calcium causes supersaturation, forming crystals.
|
|
|
|
What are some causes for kidney stones?
|
Many cases are idiopathic
50-55% have a familial tendency towards hypercalcemia or have a defect in renal tubular reabsorption of calcium. Others may have increased uric acid secretion with or without hypercalciuria. |
|
|
|
What are Staghorn calculi?
|
Struvite stones - caused by pyelonephritis caused by Proteus infections.
|
|
|
|
What are the different types of renal calculi (composition)?
|
70% - Calcium Oxalate and Phosphate
15-20% - Magnesium Ammonium Phosphate (struvite) 5-10% - Uric Acid 1-2% - Cystine +/-5% - Others/Unknown |
|
|
|
How are calculi evaluated?
|
KUB - a plain X-ray is good at visualizing stones
Urine studies - UA dipstick, microscopy, culture Intravenous Pyelogram/Urography (IVP/IVU) - dye injected through IV, rapidly fills kidneys - however, testing may hurt a compromised kidney, so make sure the BUN and creatinine are normal first. |
|
|
|
What is the imaging modality of choice for diagnosing calculi?
|
(Spiral) Non-Contrast CT - more sensitive and specific than IVP, ultrasound, fewer side effects than IVP.
Can accurately measure stone's size, degree of obstruction, exact anatomic location, other details. |
|
|
|
How do you approach treating calculi?
|
Stone </= 4mm will pass by itself 80% of the time - have patient drink lots of water, manage pain, strain urine through filter to retrieve stone and grit for analysis.
Stones 4-5mm have 40-50% chance of passing, depending on location - same Tx as above, but refer if no passage after 2 weeks. Stones >5mm should be managed by a urologist. Very low chance of spontaneous passage regardless of location. |
|
|
|
When would a calculus be a medical emergency?
|
If the patient also has anuria, renal failure, urosepsis, intractable pain, and advanced age.
|
|
|
|
How much does increasing urine volume to 2.5L/day affect stone recurrence?
|
Decreases stone recurrence by 50%
|
|
|
|
When would you use extracorporeal shock-wave lithotripsy?
|
ESWL - best with stones < 2 cm, located in the renal pelvis. Often used after debulking via percutaneous extraction. Goal is to pulverize the stone.
|
|
|
|
When is percutaneous nephrolithotomy used?
|
To retrieve large calculi or administer localized shock-wave therapy.
|
|
|
|
When is cystoscopic basket extraction used?
|
Can be used to directly retrieve calculi in the ureter
|
|
|
|
How can calcium stones be prevented?
|
Low-calcium diet is NOT effective
Thiazide diruetics decrease calcium excretion, so should adjust drugs that do that sort of thing. |
|
|
|
How can urate and cysteine stones be prevented?
|
Dietary purine restriction, allopurinol
Alkalinize the urine - take potassium citrate |
|
|
|
List three hereditary diseases of the glomerulus.
|
Alport Syndrome
Thin basement membrane disease Fabry disease |
|
|
|
What two typical characteristics tend to indicate glomerular injury?
|
Hematuria
Proteinuria |
|
|
|
Describe sustained proteinuria, and with what diseases is it associated?
|
Sustained proteinuria is 1-2gm/24h, commonly associated with glomerular disease, especially when accompanying microhematuria
|
|
|
|
Describe transient proteinuria, and with what diseases is it associated?
|
Also called functional or benign proteinuria
0.25gm/24h - 1.0gm/24h May be caused by orthostatic or postural proteinuria, fever, cold, exposure, exercise, emotional stress. |
|
|
|
What constitutes normal protein levels in the urine?
|
Less than or equal to 0.15 gm/24h
UA dip correlation = none or trace amounts In diabetics, still test for microalbuminuria |
|
|
|
What problems are associated with Proteinuria levels > 0.15gm/24h and < 3.5gm/24h?
|
Benign causes - exercise, postural proteinuria, cold exposure, fever, etc.
Nephritic syndrome Essential, uncontrolled hypertension |
|
|
|
If Proteinuria levels > 3.5gm/24h, what problems are associated with that?
|
Nephrotic syndrome
Chronic kidney disease |
|
|
|
How does UPr/Cr compare to a 24 hour urine and a urine dipstick?
|
UPr/Cr is a urine protein/creatinine ratio in a single random sample - as accurate or even more accurate sometimes than a 24 hour urine sample
Much more accurate than a urine dipstick |
|
|
|
What is the reference range for UPr/Cr?
|
< 0.2 = normal
> 3.5 = nephrotic |
|
|
|
What is a major characteristic of nephritic syndrome (compared to nephrotic)?
|
Evidence of glomerular hematuria
Suggests an inflammatory process |
|
|
|
What is a major characteristic of nephrotic syndrome (compared to nephritic)?
|
Nephrotic-range proteinuria (24h urine sample with >/= 3.5 gm of protein)
Or a UPr/Cr > 3.5 |
|
|
|
What are the basics of nephritic syndrome?
|
Inflamed glomerulus compromises blood flow and filtration
Oliguria, Hematuria, Azotemia, Hypertension, Mild Edema |
|
|
|
What are the basics of nephrotic syndrome?
|
Leaky glomerulus lets proteins out, resorption drops
> 3.5 gm/day Proteinuria, High LDL, Sever Edema, Hypoalbuminemia, Protein Foam in urine. |
|
|
|
How does one distinguish extraglomerular from glomerular hematuria?
|
Extraglomerular hematuria - urine is red or pink, clots may be present, proteinuria < 0.50 gm/day, RBC morphology is normal, RBC casts are absent
Glomerular hematuria - color is red, smoky brown "coca-cola" or tea-colored urine, clots are absent, proteinuria > 0.50 gm/day, RBCs are dysmorphic, RBC casts may be present. |
|
|
|
How are acanthocytes recognized?
|
Ring forms with vesicle-shaped protrusions
|
|
|
|
What are two ways to characterize nephritic syndrome (relating to inflammation)?
|
There is increased number of circulating inflammatory cells
An active urine sediment (indicating active inflammation) with red blood cells and possibly WBCs, RBC casts, cellular casts, granular casts Inflammatory cells may eventually block the glomerular capillaries, causing decreased renal blood flow, reduced GFR, and creatnine elevation - consistent with intrinsic ARF. Eventually there is extracellular fluid volume expansion, edema, and hypertension as kidney function declines. |
|
|
|
List several characteristics of severe nephritic syndrome.
|
Hematuria (RBC casts)
Decreased GFR Elevated serum creatinine Oliguria (<400 ml/day) Increased Na+ retention Edema Hypertension Proteinuria < 3.5 gm/day |
|
|
|
If Proteinuria levels > 3.5gm/24h, what problems are associated with that?
|
Nephrotic syndrome
Chronic kidney disease |
|
|
|
What are the major mechanisms of inflammatory injury in nephritic syndrome?
|
Immune complexes and complement activation in the mesangium or subendothelial space - IgA nephropathy, Henoch-Schonlein Purpura (high ESR), post-streptococcal glomerulonephritis (low C3, CH50; positive strep antibodies), SLE nephritis (low C3)
Auto-antibodies against the glomerular basement membrane - positive anti-GBM antibodies (Goodpasture syndrome) Antibodies against neutrophil cytoplasmic antigens - positive ANCA - systemic vasculitis (Wegeners granulomatosis) |
|
|
|
What are two major forms of antibody-associated glomerular injury?
|
Injury by antibodies reacting in situ within the glomerulus, either binding to insoluble intrinsic glomerular antigens or to molecules planted within the glomerulus
Injury resulting from deposition of circulating antigen-antibody complexes in the glomerulus |
|
|
|
How do inflammatory cells effect injury in the glomerulus?
|
The inflammatory cells block the glomerular capillaries and damage the capillary walls.
|
|
|
|
What are the mechanisms of progression in glomerular disease?
|
In many forms of glomerular disease, the triggering mechanism is self-limited or treatable, and so the patient’s long-term renal function is preserved.
In other cases, the damage progresses, causing destruction of nephrons, which causes reduction of renal mass. The patient is at risk of renal failure if the glomerular filtration rate is reduced over 30% due to nephron death. |
|
|
|
What are the two major types of progressive damage in glomerular diseases?
|
Focal segmental/global glomerulosclerosis - permanent and progressive change in the glomerulus
Tubulointerstitial fibrosis - permanent and progressive change in the tubules, distal to the glomerulus. |
|
|
|
What tests are used to evaluate suspected glomerular disorders?
|
History, Physical
Urine dipstick and urine chemistry Microscopy of urine sediment - is it an active sediment? RBC, WBC, casts, etc. Lab tests - Serum C3, CH50, anti-GBM antibody, ANA, ANCA, renal functions, CBC, etc. Strep exposure - serum for antistreptolysin O, anti-deoxyribonuclease B (anti-DNAse B), antistreptokinase (ASKase) |
|
|
|
What is the gold standard for diagnosing glomerular disorders?
|
Renal biopsy
Tissue immunofluorescence microscopy and histopathological identification - biopsy may be omitted if serology is diagnostic. |
|
|
|
Describe IgA nephropathy.
|
IgA nephropathy, also known as Berger's Disease
Most common primary glomerulopathy worldwide - 10-40% of glomerulonephritis cases. Most are idiopathic, but can be associated with chronic diseases. Diagnosis: requires renal biopsy, 50% may have low serum IgA Treatment: no definitive therapy, no known cure - fish oil? Prognosis - 20-50% progress to end-stage chronic kidney disease in 20 years |
|
|
|
What is the classic presentation of IgA nephropathy?
|
Gross hematuria, 24-48 hours after exercise, URI, GI infection, or vaccination.
Presentation ranges from benign, intermittent glomerular hematuria, to nephritic syndrome, to nephrotic syndrome. |
|
|
|
In what glomerular disease are immune complexes localized in subepithelial humps?
|
Acute glomerulonephritis
|
|
|
|
In what glomerular disease are immune complexes localized in epimembranous deposits?
|
Membranous neuropathy
Heymann glomerulonephritis |
|
|
|
In what glomerular disease are immune complexes localized in subendothelial deposits?
|
Lupus nephritis
Membranoproliferative glomerulonephritis |
|
|
|
In what glomerular disease are immune complexes localized in mesangial deposits?
|
IgA nephropathy
|
|
|
|
Describe Henoch-Schonlein Purpura.
|
HSP - most common vasculitis of childhood, median age 4.5 years
Small vessel vasculitis, IgA deposition in involved vessel walls, systemic disorder causing secondary glomerulonephritis Preceded by viral URI in ~50% of cases Classic triad: palpable purpura of the skin, arthralgias/arthritis, abdominal pain, glomerulonephritis Edema may or may not be present, skin lesions involve buttocks and lower extremities. |
|
|
|
How is Henoch-Schonlein Purpura diagnosed? Treated?
|
Diagnosis - clinical impression supported by lab findings - biopsy rarely needed
Treatment - supportive, usually a self-limited problem. NSAIDs help with joint pain, cannot use if renal function is impaired, corticosteroids for abdominal pain and nephritis, BP responds to sodium/fluid management and diuretics. |
|
|
|
What is Lupus Nephritis?
|
A common and bad complication of SLE - about 50% of SLE have renal involvement when diagnosed, 80% of children and 60% of adults eventually will. Nephritis is worst in African-American female adolescents
|
|
|
|
Describe the pathophysiology of Lupus Nephritis.
|
Deposition of circulating immune complexes in the subendothelial layer, which provokes inflammation in the glomerulus
SLE is an idiopathic AI disorder affecting multiple organs |
|
|
|
How is SLE diagnosed?
|
Screening tests - ANA (antinuclear antibody), ESR, anti-DNA antibodies, rheumatoid factor, complement levels
|
|
|
|
What are the six different classes of SLE relating to their renal histology?
|
I - Minimal mesangial - excellent prognosis
II - Mesangial proliferative - good prognosis III - Focal - moderate prognosis IV - Diffuse - moderate-poor prognosis V - Membranous - moderate prognosis VI - advanced sclerosing - poor prognosis |
|
|
|
What are some of the major characteristics of SLE?
|
Pleural effusions
Butterfly rash Raynaud's phenomenon Arthritis Lupus nephritis Heart Problems |
|
|
|
What is Goodpasture syndrome?
|
Patients develop autoantibodies directed against glomerular basement antigens and tend to also get a glomerulonephritis termed antiglomerular basement membrane (anti-GBM) disease.
When they present with lung hemorrhage and glomerulonephritis, they have a pulmonary-renal syndrome called Goodpasture syndrome. Tends to occur in men in late 20s, men and women in 60s-70s. Hemoptysis most often occurs in those who smoke. Autoantibodies cause alterations in type IV collagen |
|
|
|
How do you confirm Goodpasture syndrome?
|
Kidney biopsy is crucial to confirm the diagnosis and assess prognosis.
Evaluated for the presence of anti-GBM antibodies and complement. Serology evaluated for antineutrophil cytoplasmic autoantibody (ANCA) - which deontes a better prognosis. |
|
|
|
What treatments are available for Goodpasture syndrome?
|
Dialysis
Plasmapheresis Corticosteroids and/or Cyclophosphamide Renal transplant |
|
|
|
What is nephrotic syndrome?
|
A constellation of clinical findings resulting from massive renal losses of protein
Most common presentation is edema in the face, legs, feet, sacrum, and/or abdomen |
|
|
|
What laboratory findings are consistent with nephrotic syndrome?
|
Proteinuria > 3.5 gm/day
Non-active urine sediment (though hematuria is common) Normal serum creatinine |
|
|
|
What are the effects of urinary protein loss in nephrotic syndrome?
|
Protein loss may provoke urinary sodium retention (increased edema), and increased liver synthesis of lipids (C, TG) leading to hyperlipidemia and lipiduria
Protein loss includes immunoglobulins (increased infection risk), and antithrombin factors (hypercoagulability) |
|
|
|
List the characteristics of severe nephrotic disease.
|
Proteinuria > 3.5gm/day
Hypoalbuminemia Edema Hyponatremia Hyperlipidemia Lipiduria Hypercoagulability (thrombosis) Increased risk of infection |
|
|
|
What are the main mechanisms of injury in nephrotic syndrome?
|
Injury to epithelial cells - minimal change disease - #1 cause in children, also FSGS
Immune complex formation - membranous nephropathy - #1 cause in adults Deposition disease affecting the glomerular basement membrane |
|
|
|
What is the most common cause of nephrotic syndrome in children?
|
Minimal change disease
|
|
|
|
What is the most common cause of nephrotic syndrome in adults?
|
Membranous Nephropathy
|
|
|
|
What is the DDx for edema caused by nephrotic syndrome?
|
Nephrotic syndrome
Nephritic syndrome CHF Peripheral venous insufficiency Allergic reaction Acute renal failure Iatrogenic fluid overload |
|
|
|
What are some causes for hypoalbuminemia with edema?
|
Malnutrition
Cirrhosis Exfoliative skin disorders Protein-losing enteropathies |
|
|
|
What are some causes for hyperlipidemia?
|
Essential or family hyperlipidemia
Nephrotic syndrome |
|
|
|
Describe minimal change disease.
|
80% of nephrotic syndrome cases in children. 20% of adult cases. Peak incidence between ages 6 and 8.
Also called "nil disease" because glomerular architecture is normal under light microscopy. Electron microscope does reveal characteristic effacement of the foot processes. Most are idiopathic, with preceding viral illness. |
|
|
|
How is minimal change disease diagnosed? Treated?
|
Diagnosis - clinical impressions and labs - confirmed by response to treatment. Biopsy rare.
Treatment - corticosteroids, sometimes other medications. Long term renal function and overall survival are excellent. |
|
|
|
What is Alport syndrome?
|
A genetic condition characterized by progressive loss of kidney function and hearing (sensorineural deafness)
Eyes may be affected, 85% have X-linked inheritance, 15% autosomal recessive disease, presentation variable. In all cases - alteration in type IV collagen, may affect glomeruli, inner ear, retina |
|
|
|
What are characteristics of the renal disorder component of Alport syndrome?
|
Hematuria
Thinning and splitting of the glomerular basement membranes Mild proteinuria Chronic glomerulosclerosis Progressive kidney failure |
|
|
|
What are some treatments for Alport syndrome?
|
Control of systemic hypertension to slow the loss of renal function
|
|
|
|
What is Azotemia?
|
Defined as the retention of nitrogenous waste products (urea, creatinine) that occurs due to reduction in the glomerular filtration rate.
|
|
|
|
What is the relationship between GFR and creatinine?
|
As creatinine rises, GFR decreases
|
|
|
|
How does azotemia present with ARF vs CKD?
|
With ARF - Azotemia can occur in hours-days
With CKD - Azotemia may occur gradually over time |
|
|
|
List two ways to calculate GFR, and which is considered more accurate?
|
MDRD formula - most accurate because it has a modifier for African Americans
Cockcroft-Gault formula - requires estimate of lean body weight |
|
|
|
What is the MDRD formula?
|
GFR (mL/min/1.73m^2) = 186 x (Plasma Cr)^-1.154 x (Age)^-0.203 x (0.742 if female) x (1.210 if African American)
|
|
|
|
What is the Cockcroft-Gault formula?
|
Creatinine clearance (mL/min) = [(140-age) x lean body weight (kg)] / Plasma Cr x 72
Multiply by 0.85 for women |
|
|
|
What are the average estimated GFRs for individuals by age?
|
20-29 years = 116
30-39 years = 107 40-49 years = 99 50-59 years = 93 60-69 years = 85 70+ years = 75 |
|
|
|
What are the three general categories of acute renal failure processes?
|
Prerenal
Intrinsic Post-renal |
|
|
|
What is a prerenal process, how does it cause acute renal failure?
|
Prerenal process - diminished flow of blood to kidneys, temporarily impairing renal function. "Failure" may be temporary.
Most cases of ARF are due to prerenal processes. |
|
|
|
Corpus Callosum
|
The large band of neural fibers connecting the two brain hemispheres and carrying messages between them.
|
'Callos' sounds similar to close. The band of neural fibers connecting ("closing" the space) the brain hamispheres
|
|
|
What is a post-renal process, and how does it cause acute renal failure?
|
These obstruct flow of urine, whether in the ureters, bladder, or urethra. Like the prerenal disorders, they are usually reversible.
|
|
|
|
List some pre-renal processes that cause acute renal failure.
|
Decreased renal perfusion from...
...Decreased circulating blood volume - GI hemorrhage, diarrhea, diuretics ...Volume sequestration - Burns, pancreatitis, peritonitis, rhabdomyolysis Decreased effective arterial volume - cardiogenic shock, sepsis Reduction in CO from peripheral vasodilation - sepsis, drugs Profound renal vasoconstriction - severe heart failure, use of NSAIDs, other drugs |
|
|
|
List some intrinsic renal processes that cause acute renal failure.
|
Acute tubular necrosis - necrosis occurs when there has been prolonged renal hypoperfusion, causing ischemia to the renal tissue.
Disease of large renal vessels - renal artery stenosis, atheroembolic disease, renal vein/artery thrombosis Disease of small vessels and glomeruli - glomerulonephritis, malignant hypertension, other infectious and thrombotic disorders Disease of the tubulointerstitium - allergic interstitial nephritis, acute bilateral pyelonephritis |
|
|
|
What is the most common process that causes acute intrinsic renal failure?
|
Acute tubular necrosis
|
|
|
|
List some post-renal processes that cause acute renal failure.
|
Most common - bladder neck obstruction due to benign prostatic hypertrophy - often in conjunction with anticholinergic drugs that cause acute urinary retention.
Neurogenic bladder Nephrolithiasis (bilateral) Blood clots in the ureters or bladder neck Tumors |
|
|
|
How are acute prerenal failure and acute tubular necrosis related?
|
Prerenal ARF occurs in the setting of renal hypoperfusion - usually reversible when renal perfusion pressure is restored. Renal parenchyma is not damaged.
More severe or prolonged hypoperfusion may lead to ischemic injury, and ATN Patient can progress from a stage of reversible hypoperfusion to ischemia and necrosis, increasing the risk of long-term renal disease. |
|
|
|
What is the threshold for mean arterial pressure in the kidneys?
|
Once the mean arterial pressure falls below 80 mmHg, there is a steep decline in GFR.
|
|
|
|
Compare ischemic and toxic ATN.
|
Necrotic cells form "muddy brown" casts throughout the distal convoluted tubule.
Ischemic - In the proximal convoluted tubule and ascending/descending limbs, there is some necrosis Toxic - In the proximal convoluted tubule and ascending/descending limbs, there is a lot of necrosis |
|
|
|
How does the body react to acute prerenal failure (hypovolemia)?
|
Urine is concentrated
Avidly conserves Na+ Amount of Na+ in the filtrate is very low Maximize retention of water in the body to maximize arterial volume |
|
|
|
What kind of physiological response is present in acute intrinsic renal failure?
|
Tubules have been damaged, so there is diminished response.
|
|
|
|
How do NSAIDs affect renal function?
|
NSAIDs block prostaglandin production and can result in severe vasoconstriction of the afferent arteriole. This sabotages the kidney's ability to vasodilate as needed. Effect is hypovolemia and hypoperfusion.
|
|
|
|
How do ACE-inhibitors affect renal function?
|
They decrease efferent arteriolar tone and in turn decrease glomerular capillary perfusion pressure.
|
|
|
|
What is Chronic Kidney Disease?
|
CKD implies a spectrum of pathophysiologic processes as well as a progressive decline in GFR over time
Definition - Persistence of Azotemia for over 3 months This is the process of progressive irreversible reduction in numbers of viable nephrons and renal mass |
|
|
|
What are the two major pathologic processes that lead to the development of CKD?
|
Initiating mechanisms - such as glomerulonephritis, toxins, etc.
Progressive mechanisms, involving hyperfiltration and hypertrophy of the remaining viable nephrons following reduction of overall renal mass. |
|
|
|
What are the different stages of CKD?
|
There are 6 stages (0-5) - each marked by a GFR range (mL/min per 1.73m^3)
Stage 0 : > 90 (with risk factors) Stage 1 : >/= 90 (with demonstrated kidney damage) Stage 2 : 60-89 Stage 3 : 30-59 Stage 4 : 15-29 Stage 5 : < 15 |
|
|
|
What are some physiological and morphological changes that occur in the kidneys as CKD progresses?
|
Renal mass declines and kidneys become smaller
There is declining ability to remove toxins There is declining ability to balance sodium, potassium, and water Hyperfiltration allows excess protein to enter the infiltrate The ability to produce erythropoetin decreases causing anemia Ability to activate Vitamin D declines and bone weakens |
|
|
|
What are the two most common causes of chronic kidney disease?
|
Diabetic nephropathy
Hypertensive nephropathy |
|
|
|
What are considered risk factors for chronic kidney disease?
|
Obesity, smoking, and related risks for diabetes and hypertension
Older age African ancestry Familial history of renal disease Prior episode of ARF |
|
|
|
How does atherosclerosis develop in chronic kidney disease?
|
Early atherosclerotic injury is virtually undetectable in the systemic endothelial bed - urinary albumin excretion is a useful marker (UAE)
Oxidant stress, inflammation, and hemodynamic injury that is provoked by atherosclerosis can induce a measurable response (rise in UAE) in the renal microcirculation years before emergence of systemic disease. |
|
|
|
What is ESRD?
|
End Stage Renal Disease - characterized by development of uremic syndrome.
|
|
|
|
What are the three key processes in the pathophysiology of uremic syndrome (uremia)?
|
S/S from accumulation of toxins, including products of protein metabolism
S/S from loss of other renal functions, such as fluid and electrolyte homeostasis. Progressive inflammation which contributes to the leading cause of M/M at all stages of CKD - cardiovascular disease. |
|
|
|
What are some features of ESRD and uremia?
|
Total body sodium and water are modestly increased
Mild metabolic acidosis from declining ammonia production Fatigue, headaches, impaired mentation Skin changes - pruritis, hyperpigmentation GI - anorexia, nausea, vomiting CV - hypertension, pulmonary edema Abnormalities of serum calcium and phosphate and thinning of bone |
|
|
|
What are the major goals of management of CKD and ESRD?
|
Best possible control of diabetes and blood pressure
Smoking cessation, fixing modifiable risks Treating volume overload, bone disease, etc. Dialysis for end-stage renal disease |
|
