Clinical Manifestations of Glomerular Disease (Brozna) 1 and 2

Question 1

Kidney filters how much blood/ urine?

Answer 1

20% Cardiac Output Filters 1700 liters/day

1,000 mL urine/day

Question 2

What part of the kidney is most susceptible to ischemic injury?

Answer 2

Since the arcuate arteries do not anastomose, the central portion of the renal lobe is most susceptible to ischemic injury

Question 3

The two capillary beds

Answer 3

unique feature of renal circulation : two capillary beds arranged in series.
1. Afferent arteriole –> glomerulus (filtration of fluid and solutes).

2. via the efferent arteriole–> the peritubular capillary network (fluid and solutes reabsorbed by the tubules are returned to the circulation.)

Question 4

What is the final common pathway to end-stage renal failure?

Answer 4

Chronic hypoxia is the final common pathway to end-stage renal failure. Ischemia of the kidney is induced by the loss of peritubular capillaries in the tubulointerstitium in the late stage of renal disease

Question 5

Glomerular filter consists of

Answer 5

fenestrated endothelium, basement membrane, and foot processes of epithelial cells. Note the filtration slits and diaphragm situated between the foot processes.

Note also that the basement membrane consists of a central lamina densa, sandwiched between two looser layers, the lamina rara interna and lamina rara externa

Question 6

Assessment of renal function includes what?

Answer 6

Urine analysis
- Color, volume, cells, casts, pH, osmolality, protein, urea, creatinine, glucose

Blood examination

• Serum creatinine (used to estimate GFR, not specific)
• Blood urea (increased in many renal diseases with various glomerular, tubular or interstitial damage, not specific)

Glomerular function tests
- Glomerular filtration rate (GFR) is proportional to serum creatinine

Tubular function test

• Urine concentration test (requires water deprivation for 14 hours–> Specific gravity greater than 1.02 (normal)
• Vasopressin test

Question 7

Urine sediment: dysmorphic RBC suggests what?

White blood cell cast are most typical for what?

Answer 7

dysmorphic RBC suggests glomerular disease (it squishes through the fenestration)

White blood cell cast are most typical for acute pyelonephritis

Question 8

acute kidney injury

Answer 8

Increase in serum creatinine by ≥ 0.3mg/dLwithin 48 hours; or
Increase in serum creatinine to ≥1.5 times baseline, which is known or presumed to have occurred within the prior seven days; or
Urine volume less than 0.5mL/kg/hfor six hours

Question 9

Estimation of glomerular filtration rate through the calculation of creatinine clearance is mandatory

Answer 9

In most healthy people, the normal GFR is 90 mL/min/1.73 𝐦^𝟐 or higher.

A result of 60–89 mL/min/1.73 𝐦^𝟐 without kidney damage may be normal in some people (such as the elderly, infants).

A result of 60–89 mL/min/1.73 𝐦^(𝟐 )for three months or more, along with kidney damage (such as persistent protein in the urine), means the person has early kidney disease.

When GFR is less than 60 ml/min/1.73 m2 for 3 months or more, chronic kidney disease is present.

GFR must decline to approx half the normal level before the serum creatinine concentrtion rises above the upper limit of normal.

Question 10

Chronic Kidney Disease

Answer 10

1. Kidney damage > 3 months, as defined by structural or functional abnormalities of the kidney, with or without decreased GFR, manifested by either:
   - pathological abnormalities; or
   - Markers of kidney damage, including abnormalities in teh composition of the blood or urine, or abnormalities in imaging tests
2. GFR 3 months, with or without kidney damage

Question 11

5 stages of chronic renal failure

Answer 11

1. GFR 90+. Normal kidney function but urine findings or structural abnormalities or genetic trait point to kidney disease
2. GFR 60-89. Mildly reduced kidney function, and other findings (as for stage 1) point to kidney disease
   3a. GFR 45-59 Moderately reduced kidney function
   3b. GFR 30-44
3. GFR 15-29. Severely reduced kidney function
4. GFR less than 15 or on dialysis.

Question 12

Clinical Manifestations of Renal Diseases

Answer 12

hematuria
proteinuria
edema
hypertension
oliguria
anuria
increased serum 	creatinine
increased serum 	BUN
mass

Question 13

Uroscopy

Answer 13

is the histologic medical practice of visually examining a patient’s urine for pus, blood or other symptoms of disease. It dates back to ancient Egypt Babylon and India

Question 14

13th century description of symptoms of chronic nephritis

Answer 14

The signs of hardness in the kidneys are that the quantity of the urine is diminished, that there is heaviness of the kidneys, and of the spine with some pain: and the belly begins to swell up after a time and dropsy is produced the second day…

Question 15

foamy urine is associated with

Answer 15

proteinuria

Question 16

Bright Disease

Answer 16

= Glomerulonephritis

In 19th century Bright Disease became known as a chronic but incurable disorder… along with tuberculosis and cancer as diagnoses that could extinguish all hope and interest in life

Bright Disease was the FEARED disease of the 1800s

Question 17

What the microscope and labs of late 1800s said about Bright disease

Answer 17

Acute form of Bright disease that made urine bloody as well as albuminuric, caused flank pain and was associated with blood engorged swollen kidneys –> Acute glomerulonephritis

Bright disease dominated by extreme albuminuria and stubborn dropsy, large pale kidneys –> Nephrotic syndrome

Bright disease arising from narrowing and hardening of the kidneys’ arterial network –> Vascular kidney diseases

Question 18

4 groups of kidney pathology

Answer 18

Can divide kidney diseases into those that affect the basic morphologic components:
Blood vessels
Tubules
Interstitium 
Glomeruli

Early manifestations of disease affecting each of these components tend to be distinct and some components seem to be more vulnerable to specific forms of renal injury
For example:
Most glomerular diseases are immunologically mediated.

Question 19

Pathogenesis of Glomerular Injury

Answer 19

• Most forms of human glomerulonephritis result from immunologic mechanisms
• Most precipitating factors initiate similar immune responses that result in glomerulonephritis via shared common pathways
• Most human glomerular diseases are characterized by glomerular immunoglobulin deposition +/- complement
• Immune deposits form either actively (AbAg) or passively as exogenous antigens become trapped in glomerulus due to glomerular filtration

Question 20

Two forms of antibody-associated injury have been established:

Answer 20

Injury byantibodies reacting in situ within the glomerulus,either binding to insoluble fixed (intrinsic) glomerular antigens or extrinsic molecules planted within the glomerulus.

Injury resulting from deposition of circulating antigen-antibody complexes in the glomerulus.

*** the major cause of glomerulonephritis resulting from formation of antigen-antibody complexes is in situ immune complex formation, and not deposition of circulating complexes.

Question 21

Pathogenesis of Glomerular Injury

Answer 21

Cellular immunity can lead to the production of cytokines
Cause the glomerular basement membrane to lose its negative charge
Damage podocytes causing the process fusion
Mesangial cell proliferation and matrix formation

Question 22

Podocytes, mesangial cells, endothelial cells interact with each other

Answer 22

Growth factors
Cytokines
Vasoactive agents
Chemokines
Complement receptors

Podocyte injury frequently results in mesangial cell proliferation, whereas mesangial cell injury leads to foot process fusion and proteinuria

Question 23

Four Types of Immune Reactions

Answer 23

Type I immune reaction (anaphylactic)
Hypersensitivity reaction mediated by IgE which occurs relatively rapidly following exposure to previously encountered antigen

Type II immune reaction (antibody mediated)
Caused by antibodies which react with self-antigens

Type III immune reaction ( immune complex mediated)
Involve the deposition of preformed immune complex which result in complement activation

Type IV immune reaction (delayed hypersensitivity cell-mediated)
Mediated predominantly by T cells

Question 24

In situ Formation of Immune Complexes in the Glomerulus

Answer 24

Intrinsic antigens in the glomerulus
Antibody to glomerular basement membrane –> Goodpasture disease
Antibody to phospholipase A2 receptor –> Membranous nephropathy

Extrinsic antigens trapped (planted) in the glomerulus
Cationic molecules
Nuclear proteins
Infectious agent antigens

Question 25

Deposition of Circulating Immune Complexes

Answer 25

Glomerular injury can be caused by the trapping of circulating immune complex Immune complex antigens may be of endogenous origin DNA, tumor antigens ``` Immune complex antigen may be of exogenous origin Microbial antigens (streptococcal proteins) Viral antigens (hepatitis virus) ```

Question 26

Immune Complex Localization

Answer 26

Several factors affect glomerular localization of antigen, antibody or complexes: Molecular charge and size Cationic molecules tend to cross glomerular basement membrane and deposit in sub-epithelial location Anionic molecules are excluded from the basement membrane and localized in sub-endothelial locations Neutral charge antigens or complexes tend to accumulate in the mesangium

Question 27

Antibody mediated immune injury

Answer 27

Immune complex formation leads to complement activation and activation of leukocyte mediated injury pathways

Question 28

Primary Renal Disease

Answer 28

Pathologic changes in the kidney in the absence of associated systemic disease Only kidneys are affected

Question 29

Secondary Renal Disease

Answer 29

``` Systemic disease causes the renal disease Diabetes mellitus Systemic lupus erythematosus Hypertension Amyloidosis ```

Question 30

Terms used to Describe | Histologic Lesions in Glomeruli

Answer 30

Focal- Involving less than 50% of glomeruli Diffuse- involving > 50% of glomeruli Segmental- involving part of a glomerular tuft Global- involving all of a glomerular tuft

Question 31

Acute renal failure

Answer 31

Oliguria or anuria (reduced or no urine flow) Recent onset of progressive azotemia Overwhelming majority due to “Acute Kidney Injury” (acute tubular necrosis) but some cases may be the result of vascular or extensive glomerular injury. interstitial, or vascular injury or acute tubular injury.

Question 32

Chronic renal failure

Answer 32

Prolonged symptoms and signs of uremia End result of all progressive chronic parenchymal renal diseases Also termed “End Stage Renal Disease” (ESRD)”

Question 33

Glomerular immunopathology often develops from

Answer 33

intra-glomerular complement activation via the classical (immune complex-related) or alternative (immune complex independent) complement pathway Immune complexes can form in different compartments of the glomerulus, which determines the resulting histopathological lesion, as different glomerular cell types are primarily activated in each compartment

Question 34

Can divide kidney diseases into those that affect the basic morphologic components:

Answer 34

Blood vessels Tubules Interstitium Glomeruli

Question 35

Clinical Presentation of Vascular Kidney Diseases

Answer 35

Benign nephrosclerosis Slight drop in GFR and mild proteinuria Malignant nephrosclerosis Rapidly increasing blood pressure, increased intracranial pressure with headaches, papilledema and retinal hemorrhages Thrombotic microangiopathies Microangiopathic hemolytic anemia (DIC) Hemolytic uremic syndrome (HUS) Thrombotic thrombocytopenic purpura (TTP)

Question 36

Clinical Presentations of Tubular and Interstitial Kidney Diseases

Answer 36

Acute interstitial nephritis (uncommon) Sudden onset and rapid decline in renal function Immunologic hypersensitivity reaction (drug or infectious agent) Chronic interstitial nephritis Protracted onset and slow decline in renal function (progressive scarring) Toxins, drugs, infections, obstruction, immunologic and ischemia Acute tubular injury/necrosis (ATN) Sudden onset and rapid decline in renal function Ischemia and direct toxic injury to the tubules

Question 37

Clinical Presentations of Glomerular Kidney Diseases

Answer 37

Asymptomatic hematuria and / or proteinuria Macroscopic hematuria Nephritic syndrome (Glomerulonephritis) Nephrotic syndrome Rapidly progressive glomerulonephritis Chronic glomerulonephritis (chronic kidney disease)

Question 38

Asymptomatic hematuria/proteinuria

Answer 38

Proteinuria 150 mg to 3 g per day Hematuria >2 red blood cells per high-power field in spun urine MOST hematuria is Not glomerular in origin

Question 39

Macroscopic hematuria

Answer 39

Brown/red painless hematuria Asymptomatic hematuria + proteinuria between attacks of hematuria MOST hematuria is Not glomerular in origin

Question 40

Nephritic syndrome clinical presentations

Answer 40

``` Oliguria Hematuria with red cell casts Proteinuria usually less than 3 g/day edema hypertension abrupt onset and usually self-limiting ```

Question 41

Nephrotic syndrome clinical presentations

Answer 41

``` Proteinuria >3.5 g per day (adult); >40mg/hr per m2 (child) Hypoalbuminemia less than 3.5 g/dl Edema Hypercholesterolemia Lipiduria ```

Question 42

Rapidly progressive glomerulonephritis

Answer 42

``` Renal failure over days to weeks Proteinuria usually less than 3 g/day Hematuria with red cell casts may have features of vasculitis blood pressure often normal ```

Question 43

Chronic glomerulonephritis (chronic kidney disease)

Answer 43

Hypertension ** Renal impairment (GFR impairment (GFR less than 60 ml/min for 3 months) Proteinuria usually less than 3 g/day Shrunken smooth kidneys

Question 44

Histopathologic Classification of Glomerulonephritis-- Heptinstall’s Pathology of the Kidney. These are histological patterns, not diagnoses

Answer 44

No abnormality by light microscopy Thick capillary walls without hypercellularity or mesangial expansion Thick walls with mesangial expansion but no hypercellularity Focal segmental glomerulosclerosis without hypercellularity Mesangial or endocapillary hypercellularity Extracapillary hypercellularity Membranoproliferative, lobular or nodular pattern Advanced diffuse global glomerular sclerosis

Question 45

No abnormality by light microscopy

Answer 45

Glomerular disease with no light microscopic changes (e.g., minimal change glomerulopathy, thin basement membrane nephropathy) Mild or early glomerular disease (biopsy sampling) (e.g., lupus nephritis, IgA nephropathy, membranous glomerulopathy, amyloidosis, etc.)

Question 46

Focal segmental glomerulosclerosis

Answer 46

Focal segmental glomerular sclerosis is clinicopathologic term used to describe steroid resistant nephrotic syndrome in children and adolescents

Question 47

TO Determine the cause of a patient’s kidney disease need...

Answer 47

integration of data from light microscopy, immunofluorescence microscopy, electron microscopy, serology, and other laboratory and clinical observations

Question 48

Microscopic hematuria with proteinuria

Answer 48

Much greater risk of significant glomerular injury and renal biopsy is indicated

Question 49

**Isolated non-nephrotic proteinuria

Answer 49

Functional proteinuria: Orthostatic (postural) proteinuria (children and young adults), Transient proteinuria (fever, exercise common in young individuals) Acute illnesses Dehydration May be an early sign of a serious glomerular or tubular lesion **Normal urinary sediment, no hematuria, normal GFR, no hypertension, no diabetes

Question 50

Microscopic hematuria

Answer 50

(common in children and adults) Urologic origin 80% (bladder, ureters, prostate) if no proteinuria Strenuous exercise or unexplained with no urologic findings Differential of glomerular hematuria without proteinuria, renal insufficiency or red blood cell casts Thin basement membrane nephropathy (benign familial hematuria) Alport syndrome (familial) IgA nephropathy

Question 51

Confirm Microscopic Hematuria

Answer 51

Microscopic hematuria is usually defined as >3-5 RBC/hpf Cannot use urine dipstick alone (false positives- myoglobin, bilirubin) Prevalence of microscopic hematuria in schoolchildren ~2-4% on one urinalysis  0.4% after 4 UA in 1 year > 70% of children with isolated microscopic hematuria on a single UA will not have persistent hematuria after further testing

Question 52

Urine sediment: | Red blood cells with normal morphology

Answer 52

Extraglomerular origin Hypercalciuria Urethra injury Cystitis

Question 53

Urine sediment: | Dysmorphic red blood cells

Answer 53

Glomerular origin IgA nephropathy Alport syndrome Thin glomerular basement membrane disease

Question 54

Thin Basement Membrane Nephropathy

Answer 54

(Benign Familial Hematuria) Diffuse thinning of glomerular basement membrane Normal light microscopy and immunofluorescence Persistent microscopic hematuria (also episodic macroscopic hematuria) Affects 1% of general population (autosomal dominant) Most present with only hematuria (mild proteinuria may be present) Normal renal function and excellent prognosis (risk of progression

Question 55

Alport Syndrome

Answer 55

(Hereditary Nephritis) ``` Inherited disorders of basement membranes (mutations of type IV collagen alpha chain proteins) Major clinical features Hematuria Progressive nephritis with proteinuria Declining renal function Sensorineural deafness Ocular abnormalities ``` Clinical course is gender dependent Affected males have severe disease Affected females have mild disease Fine structural feature of the kidney that occurs in most patients with AS is the variable thickening, thinning, and splitting/lamellation of the GBM  No pathognomonic lesions by light microscopy Glomerular basement membrane fails to stain by immunofluorescence for α3, α4, α5 *** Type IV collagen chains

Question 56

IgA nephropathy

Answer 56

IgA nephropathy also can also present with macroscopic hematuria (Berger disease) is characterized by IgA deposits in the mesangial regions and is the most common type of glomerulonephritis worldwide Episodic gross hematuria occurring within 1 day of acute respiratory infection (50% of children) Major clinical presentations are episodic macroscopic hematuria with persistent microscopic hematuria 40 to 50% present with one or recurrent episodes of visible hematuria following upper respiratory infection Most have only a few episodes of visible hematuria and episodes usually recur for only a few years. 30 to 40% have microscopic hematuria and mild proteinuria Gross hematuria will eventually occur in 20 to 25 percent of these patients Disease of uncertain duration 5-10% present with either nephritic syndrome or acute rapidly progressive glomerulonephritis

Question 57

Episodic Painless Macroscopic Hematuria Caused by Glomerular Disease

Answer 57

Observed primarily in children and young adults and less commonly past age of 40 Most cases are caused by IgA nephropathy

Question 58

IgA Vasculitis

Answer 58

Henoch-Schönlein purpura (HSP) is a small-vessel vasculitis affecting the skin, joints, gut, and kidneys that predominantly affects children Most children have mild illness that resolves spontaneously Tissue deposition of IgA Skin rash (palpable purpura) RARE Intestinal bleeding or intussusception Nephritis associated with HSP is characterized by mesangial IgA deposition and is indistinguishable from IgA nephropathy

Question 59

IgA Nephropathy Pathogenesis Theory

Answer 59

IgA glomerular deposits are predominantly polymeric IgA Levels of plasma polymeric IgA are increased Aberrant glycosylation of IgA Direct deposit of glycosylated IgA or deposit of immune complex of IgA and IgG anti IgA Alternate pathway of complement activation with C3 deposits usually in the absence of C1q and C4 **The regular recurrence of IgA nephropathy and Henoch-Scholein purpora nephritis after renal transplantation strongly implies an abnormality in the host IgA immune system

Question 60

Nephritic syndrome

Answer 60

``` Hematuria with red cell casts Proteinuria usually less than 3 g/day Edema Hypertension Oliguria (low urine output) Azotemia Abrupt onset and frequently self-limiting ```

Question 61

Histological features of kidney diseases

Answer 61

Acute proliferative glomerulonephritis - poststreptococcal glomerulonephritis - postinfectious glomerulonephritis Focal proliferative glomerulonephritis - lupus nephritis - IgA nephropathy Diffuse proliferative glomerulonephritis - lupus nephritis - Goodpasture’s nephritis - vasculitis induced glomerulonephritis - membranoproliferative glomerulonephritis - crescentic glomerulonephritis

Question 62

Acute Proliferative Glomerulonephritis(Post-streptococcal Glomerulonephritis)

Answer 62

Beta hemolytic group A streptococcus specific nephritogenic strains are capable of inducing acute post-streptococcal glomerulonephritis Streptococcal pyogenic exotoxin B (SPE B) probably major antigen involved in the pathogenesis of most cases of APSGN. Follows upper-respiratory tract infections, such as pharyngitis or tonsillitis and skin infections (impetigo) Most commonly affects children and young adults Variable clinical presentation from asymptomatic microscopic hematuria to the full-blown acute nephritic syndrome that may progress Onset of clinical symptoms is typically abrupt 1- 3 weeks after upper respiratory group A streptococcal infection; (3-6 weeks after skin infection, impetigo) ``` Classic presentation is acute nephritic syndrome Hematuria (100%); Gross hematuria (30%) Edema Hypertension Proteinuria ``` Variable decline in glomerular filtration (rise in serum creatinine)

Question 63

Acute proliferative glomerulonephritis(post-streptococcal) : Children vs Adults

Answer 63

Children tend to clear in 6 –8 weeks – renal biopsy not generally indicated 95% recover completely with conservative therapy (water and salt restriction); no long term sequellae

Question 64

Acute Proliferative Glomerulonephritis(Poststreptococcal Glomerulonephritis) Pathologic Features

Answer 64

All glomeruli are affected (Diffuse) -Patients who are asymptomatic or have mild disease may have biopsies that show little glomerular involvement, whereas patients with diffuse endocapillary proliferative glomerulonephritis are more likely to have full-blown acute nephritic syndrome Acute proliferative glomerulonephritis - Proliferation of mesangial and endothelial cells - Interstitial infiltrates of lymphocytes, monocytes and neutrophils Glomerular immune deposits (immune complexes) - Complement (C3) - 100% - Immunoglobulin G or M -~60-70% Residual renal injury is common in older adults (Focal glomerular sclerosis and mesangial expansion)

Question 65

Poststreptococcal glomerulonephritis (PSGN) is usually diagnosed based upon the presence of:

Answer 65

``` Acute nephritic symptoms Virtually all patients present with microscopic hematuria Gross hematuria (30%) Edema Hypertension Proteinuria AND Recent group A beta hemolytic streptococcal infection ``` Renal biopsy is not performed in most patients to confirm the diagnosis of PSGN, since the resolution of PSGN typically begins within one week of presentation.

Question 66

Acute proliferative glomerulonephritis(Post-infectious, Non-streptococcal)

Answer 66

Staphylococcus-associated glomerulonephritis is as common as post-streptococcal glomerulonephritis in adults Most of the other causes of bacterial infection-associated glomerulonephritis, including that due to Staphylococcus infection occur when the patient is still infected. Immune complex mediated disease (thought to be preformed complexes) Often IgA antibody to staphylococcal antigen Hepatitis virus B and C and HIV can be associated with postinfectious acute proliferative glomerulonephritis Parasites (malaria, toxoplasmosis) can be associated with postinfectious acute proliferative glomerulonephritis

Question 67

Membranoproliferative Glomerulonephritis synonym: Mesangiocapillary Glomerulonephritis

Answer 67

Includes pathologically distinct forms of glomerulonephritis: Immune complex mediated disease (Type 1 MPGN) *** Subendothelial dense deposits and splitting of GBM Complement mediated disease (Dense Deposit Disease) *** Dense intramembranous deposits, formally type II MPGN Accounts for 10% of nephrotic syndrome in children and young adults (Type 1 more frequent than dense deposit disease)

Question 68

Clinical findings of membranoproliferative glomerulonephritis

Answer 68

range from microscopic hematuria with or without mild proteinuria to nephrotic syndrome and severe glomerulonephritis with hypertension and reduced GFR. (Combined nephritic/nephrotic pattern)

Question 69

Type 1 MPGN

Answer 69

Most have either subendothelial and/or mesangial immune complex deposits (antigens are unknown) Thought to be infectious agent antigens trapped in glomeruli ~ 1/3 will have circulating immune complexes Thickened GBM with double contour (tram-tracking) Most present as adolescents or young adults Approximately two thirds of the patients develop hypocomplementemia with predominant depletion in C3 levels Approximately 50% progress to chronic renal failure within 10 years

Question 70

Dense Deposit Disease

Answer 70

Often has light microscopic features that resemble MPGN type I, dense deposit disease is also called type II MPGN. Less common than type 1 MPGN Most are persistent C3 activation (70% of patients)

Question 71

Histological aspects of membranoproliferative glomerulonephritis

Answer 71

Thickening of capillary walls, usually global and diffuse. There is also hypercellularity. Much of this hypercellularity is mesangial proliferation, and some of the capillary wall thickening is caused by mesangial interposition into the subendothelial zone of the capillary loops.

Question 72

Nephritic Syndrome Children/Adolescents

Answer 72

IgA glomerulopathy Post-streptococcal glomerulonephritis Hemolytic uremic syndrome (Thrombotic microangiopathy) Henoch-Schonlein purpura (IgA nephropathy) Membranoproliferative glomerulonephritis (nephritic / nephrotic presentations)

Question 73

Nephritic Syndrome Adults

Answer 73

IgA nephropathy Goodpasture syndrome Post-streptococcal glomerulonephritis Diffuse proliferative glomerulonephritis (eg Lupus) Rapidly progressive crescentic glomerulonephritis Membranoproliferative glomerulonephritis (nephritic / nephrotic presentations)

Question 74

Key concepts of nephritic syndrome

Answer 74

Acute postinfectious glomerulonephritis prototypic example of nephritic syndrome Rapidly progressive glomerulonephritis- nephritic syndrome and rapid loss of renal function

Question 75

3 things that change the GFR calculation

Answer 75

Age, female, african american