4 CKD And Nephrotic Syndrome Flashcards

1
Q

What is the most common comorbid condition with CKD?

A

Diabetes

Continues to be the leading cause of ESRD

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2
Q

Gender difference in CKD prevalence

A

Women more commonly affected (18% vs 13%) but men tend to have more progressive course

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3
Q

What is the definition of CKD?

A

Decreased kidney function or kidney damage for 3 or more months

Glomerular filtration rate (GFR) < 60 mL/min/1.73m2

Evidence of kidney damage:
• Albuminuria*** Urine albumin:Cr ratio of ≥30 mg/g
• Abnormal imaging tests (U/S)
• Abnormal urinary sediment (ie RBC casts)
• Hx of kidney transplant

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4
Q

What is the best marker of kidney function?

A

GFR - declining GFR is the hallmark of progressive kidney disease

Serum creatinine is a poor measure of kidney function

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5
Q

Name the CKD Stage:

Kidney damage with normal or increased GFR (≥ 90)

A

Stage 1

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6
Q

Name the CKD Stage:

Kidney damage with mildly decreased GFR (60-89)

A

Stage 2

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7
Q

Name the CKD Stage:

Mildly-moderately decreased GFR (45-59)

A

Stage 3a

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8
Q

Name the CKD Stage:

Moderately-severely decreased GFR (30-44)

A

Stage 3b

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9
Q

Name the CKD Stage:

Severely decreased GFR (15-29)

A

Stage 4

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10
Q

Name the CKD Stage:

Kidney failure, GFR < 15

A

Stage 5 - add D if treated by dialysis

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11
Q

Name the Albuminuria classification:

ACR < 30 mg/g
Protein dipstick - negative to trace

A

Stage A1

Normal to mildly increased

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12
Q

Name the Albuminuria classification:

ACR 30-300 mg/g
Protein dipstick trace to 1+

A

Stage A2

Moderately increased

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13
Q

Name the Albuminuria classification:

ACR > 300mg/g
Protein dipstick >1+

A

Stage A3

Severely increased

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14
Q

What is important to know about measuring Albuminuria?

A

Must be verified by a repeated test - it has to be PERSISTENT over several months

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15
Q

What is the pathogenesis of CKD?

A

Progressive decline in the GFR typically over months to years, due to the IRREVERSIBLE DESTRUCTION OF NEPHRONS INDEPENDENT of the cause (still need to ID the cause though)

Destruction of nephrons leads to COMPENSATORY HYPERTROPHY and supranormal GFR of the remaining nephrons

Compensatory hyperfiltration leads to OVERWORK INJURY in the remaining nephrons

Progressive GLOMERULAR SCLEROSIS and INTERSTITIAL FIBROSIS

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16
Q

Because of the progressive nephron and GFR loss, what will you see in lab results?

A

Abnormalities in water, electrolyte, and pH balance

Accumulation of waste products normally excreted

Abnormalities in the production and metabolism of certain hormones (EPO, calcitriol)

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17
Q

What are the most common causes of CKD?

A

DIABETES

HTN

Glomerular disease

Polycystic kidney disease

Chronic Tubulointerstitial disorders

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18
Q

How should you screen patients at risk for developing CKD?

A

Urine albumin-to-creatinine ratio

Serum creatinine to estimate GFR (eGFR)

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19
Q

Who IS at risk for CKD?

A
60 years or older
Diabetes
HTN
CVD
FHx of kidney disease
Ethnic minority
Cancer
Systemic infection (HIV or Hep C)
Recurrent UTIs
Nephrolithiasis
Nephrotoxic drug exposure
Autoimmune disorders
Hx of AKI
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20
Q

What is the clinical presentation of CKD?

A

Dependent on underlying cause and stage

Sx develop slowly with the progressive decline in GFR

Asymptomatic in early stages

Sx may not manifest until kidney failure is far advanced

Nonspecific Sx - fatigue, for example - worry about uremic syndrome

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21
Q

Accumulation of metabolic waste products, or uremic toxins

A

Uremic syndrome

Often seen with a profound decrease in GFR (10-15 mL/min/1.73m2)

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22
Q

What are the SSx of uremic syndrome?

A

FATIGUE, MALAISE, anorexia, N/V

Pruritis, easy bruisability

Metallic taste in mouth

Shortness of breath

Dyspnea on exertion, PERICARDITIS

Restless legs, seizures, ENCEPHALOPATHY

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23
Q

What finding on renal U/S supports a diagnosis of CKD?

A

Small kidneys BL (<9-10cm) - decline in renal mass/atrophy

Although normal or enlarged kidneys may be seen as well

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24
Q

_________ may lead to death before the progression to ESRD

A

Complications of CKD

More likely to occur at later stages - why you need to ID complications early

May arise from the adverse effects of interventions used to prevent or treat

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25
Q

What are the main complications of CKD?

A

CARDIOVASCULAR DISEASE - a leading cause of death

HTN

Dyslipidemia

Anemia (b/c kidneys —> EPO)

Mineral/bone disorders

Fluid and electrolyte abnormalities (hyperkalemia, hyperphosphatemia, hypocalcemia, metabolic acidosis)

Uremia

Malnutrition (low serum albumin)

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26
Q

Spectrum of bone disorders that are a complication of CKD

A

Osteitis fibrosa cystica, adynamic bone disease, osteomalacia (bone remodeling and demineralization)

Typical pattern: hyperphosphatemia, hypocalcemia, decreased vitamin D, SECONDARY HYPERPARATHYROIDISM

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27
Q

CKD Mineral and Bone Disorder is often clinically detectable starting at what stage?

A

Stage 3 CKD

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28
Q

What are the keys to managing CKD?

A

IDENTIFY THE CAUSE

Identify and treat potentially reversible factors

Manage complications

Frequent review of meds (avoid nephrotoxic drugs, adjust drug doses when appropriate)

Identify and adequately prepare the patient in whom renal replacement therapy will be required

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29
Q

Reversible causes of kidney injury

A

Infection (do a urine culture/sensitivity)

Obstruction*** (bladder cath, renal US)

Volume depletion (BP, pulse, orthostatic measurements)

Nephrotoxic agents (drug history, recent imaging)

Heart failure (phys exam, CXR)

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30
Q

How do you slow the progression of CKD?

A

TREATMENT OF THE UNDERLYING CAUSE OF CKD

Glycemic control

BP control - ACE/ARBS to reduce proteinuria, low sodium diet

Weight management

Management of CV risk factors (statins, smoking cessation)

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31
Q

Why are ACE/ARBs so great for CKD patients?

A

RENOPROTECTIVE

Helpful in SLOWING THE PROGRESSION OF PROTEINURIC CKD (lowers albuminuria) in chronic stable patients

Inhibiting Ang II —> DILATES the EFFERENT arteriole —> reducing glomerular pressure

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32
Q

When are ACE/ARBs HARMFUL for CKD patients?

A

May see an acute reduction in GFR and hyperkalemia - ok in chronic states but a problem in acute settings

Use with caution in AKI

Contraindicated in bilateral renal artery stenosis***

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33
Q

What are the BP targets in patients with CKD?

A

In patients without proteinuria, target is <140/90

In patients WITH proteinuria, target is <130/80

Tailor BP treatment in elderly patients with CKD

34
Q

When should you refer a CKD patient to nephrology?

A

GFR <30

35
Q

Other than looking at GFR, why might we refer patients to nephrology?

A

To determine the cause of CKD (regardless of GFR)

Management of complications
• EPO Therapy
• CKD-MBD —> phosphate binders
• Resistant HTN

Preparation for and initiation of dialysis

Transplant evaluation

36
Q

What are the options for renal replacement therapy?

A

Dialysis
• Hemodialysis
• Peritoneal dialysis

Kidney transplant

37
Q

Indications for dialysis for CKD

A

Uremic symptoms
Fluid overload unresponsive to diuresis
Refractory hyperkalemia, acidosis, and hyperphosphatemia

Prepare early (GFR <30) as it takes time to set up an AV fistula

38
Q

How is hemodialysis conducted?

A

Requires a constant flow of blood along one side of a SEMIPERMEABLE MEMBRANE with a cleansing solution, or a DIALYSATE, along the other

Diffusion and convection allow the dialysate to REMOVE UNWANTED SUBSTANCES from teh blood while adding back needed components

39
Q

What are the acute complications of hemodialysis?

A

HYPOTENSION (25-55% of treatments) due to overfiltration

Cramps
N/V
HA
Chest pain
Back pain
Itching
Fever and chills
40
Q

In Peritoneal Dialysis, the ________ is the dialyzer.

A

Peritoneal membrane

DIALYSATE is instilled into the peritoneal cavity via an in dwelling catheter

Peritoneal membrane acts as a partially permeable membrane and diffusion and osmosis drive waste products and excess fluid through the peritoneum into the dialysate

After equilibrium, the dialysate is drained, discarded, and replaced with fresh dialysate

41
Q

What are the complications of peritoneal dialysis?

A

PERITONITIS*****
Exit site infection
Poor dialysate drainage

42
Q

What is the treatment of choice for ESRD?

A

Kidney transplant

Improved quality of life

Reduces the mortality risk for most when compared to maintenance dialysis - but not all are medically suitable for transplant

43
Q

What is chronic Tubulointerstitial disease?

A

Chronic disease associated with insults from an acute factor or progressive insults without any obvious acute cause

44
Q

Interstitial scarring, fibrosis, and tubular atrophy leading to a progressive decrease in eGFR (CKD)

A

Chronic Tubulointerstitial Disease

45
Q

Underlying etiologies of Chronic Tubulointerstitial Disease

A

Obstructive uropathy***

Reflux nephropathy***

Analgesic nephropathy

Heavy metals (lead)

Lithium

46
Q

General findings of chronic Tubulointerstitial diseases

A

Polyuria due to inability to concentrate the urine secondary to tubular damage

Hyperkalemia due to decreased GFR as distal tubules become aldosterone resistant

U/A is nonspecific, but will have PROTEINURIA (<2g/d), broad waxy casts indicating dilated, damaged tubules

47
Q

Prolonged obstruction of the urinary tract —> reduced GFR, reduced renal blood flow, and impaired tubular function

A

Obstructive uropathy

Tubular atrophy, interstitial fibrosis and eventually irreversible renal injury occur

Not always symptomatic depending on degree/type of obstruction

If you catch obstruction within a week or so it’s reversible

48
Q

Examples of urinary tract obstructions that can lead to obstructive uropathy

A

Prostatic disease

Urethral calculus in a single functioning kidney

BL urethral calculi

Carcinoma of the cervix, colon, or bladder

Retroperitoneal tumors or fibrosis

49
Q

What will labs/imaging show that suggests obstructive uropathy?

A

UA - may show hematuria, pyuria, and bacteriuria, but often benign

U/S - detect mass, hydroureter, hydronephrosis

50
Q

The consequence of vesicoureteral reflux (VUR) or other urologic anomalies in early childhood

A

Reflux Nephropathy

Incompetent vesicoureteral sphincter —> urine can extravasated into the interstitium —> inflammatory response develops (either bacteria or normal urinary components) —> FIBROSIS occurs

51
Q

When is Reflux Nephropathy usually diagnosed?

A

In young children with a Hx of recurrent UTIs

May go unnoticed until early adulthood, when it often presents with HTN

Dx is via RUS (showing scarring and hydronephrosis) and VCUG

52
Q

CKD caused by LONG TERM, excessive consumption of analgesics, often when taken in combination medications

A

Analgesic Nephropathy

Example meds - acetaminophen and NSAIDs (ie excedrin)

Seen often with those who are using analgesics for chronic headaches, muscular pains, and arthritis

53
Q

What do diagnostics look like for analgesic nephropathy?

A

UA —> hematuria, mild proteinuria, sterile pyuria (WBC but no bacteria)

CT scan —> papillary microcalcifications/necrosis

54
Q

What are the key points in the treatment of Chronic Tubulointerstitial Disorders?

A

Identify the underlying disorder

Medical management

Relief of obstruction

Withdrawal of all analgesics

Referral to nephrology or urology

55
Q

Non inflammatory damage to the glomerular capillary wall (podocyte and GBM) that can be either primary or in association with a systemic disease

A

Nephrotic Syndrome

Nephritic Spectrum = Diseases that present primarily with PROTEINURIA and a bland urine sediment (no cells or cellular casts

56
Q

What are the distinct constellation of clinical and lab features of renal disease that make up Nephrotic Syndrome?

A

Nephrotic-range proteinuria (>3.5g/day), Hypoalbuminemia, Edema, Hyperlipidemia

57
Q

Urine features in Nephrotic vs Nephritic Syndrome

A

Nephrotic = “Foamy”, oval fat bodies

Nephritic = cola-colored urine with RBC casts

58
Q

Primary causes of Nephrotic Syndrome

A

Minimal Change Disease (MCD)
Membranous Nephropathy (MN)
Focal Segmental Glomerulosclerosis (FSGS)

59
Q

Secondary causes of Nephrotic Syndrome

A

DIABETIC NEPHROPATHY

Amyloidosis

60
Q

SSx of Nephrotic Syndrome

A

EDEMA (periorbital, pedal, anasarca)

ASCITES

FOAMY URINE (from excess protein)

Malaise, Anorexia, Dyspnea, Abdominal distension, Weight gain, Orthostatic hypotension from hypovolemia

61
Q

Complications of Nephrotic Syndrome

A

Protein malnutrition

HYPERCOAGULABILITY (urinary loss of antithrombin, protein C/S, increased platelet activation)

Vitamin D deficiency and hypocalcemia (urinary loss of vitamin D binding protein)

INFECTION (urinary loss of immunoglobulins, defect in the complement cascade)

Anemia (urinary loss of EPO and transferrin)

62
Q

Pathognomic urine microscopy finding suggestive of nephrotic syndrome

A

OVAL FAT BODY

63
Q

How is Nephrotic Syndrome managed?

A

ACE/ARBs

Statin therapy

Loop diuretics

Sodium/fluid restriction

Anticoagulants when indicated (ie evidence of VTE)

Immunosuppressive therapy (corticosteroids, cytotoxic agents)

Nephrology referral

64
Q

Most common cause of nephrotic syndrome in CHILDREN

A

Minimal Change Disease (MCD)

M>F, peaks at age 2 years

65
Q

Most cases of MCD are idiopathic primary, but secondary MCD can be associated with…

A

Following an URI** (esp in children), hypersensitivity reactions (NSAIDS, bee stings), meds (lithium), malignancies (Hodgkin disease)

66
Q

How does MCD usually present?

A

SUDDEN ONSET of edema (“Puffy appearance”) over days to a week or two

No changes on light microscopy

Primarily affects the PODOCYTE (diffuse podocyte foot process fusion) - visible on ELECTRON MICROSCOPY

67
Q

What is the first line treatment for MCD?

A

Prednisone - works well, well tolerated

Very few patients progress to ESRD

68
Q

One of the more common forms of nephrotic syndrome in the adult population, with peak around the fourth and fifth decades, M>F

A

Membranous Nephropathy (MN)

Most often a primary idiopathic disorder in adults

Primary MN - thought to be IMMUNE-MEDIATED, with autoantibodies directed against an antigen found on the podocytes

Secondary MN - can be due to Hep B, autoimmune diseases, thyroiditis, malignancy, drugs

69
Q

How does Membranous Nephropathy present?

A

GRADUAL development of features of nephrotic syndrome, with a higher risk of hypercoagulable state

~20-40% will get a clot or renal vein thrombosis

Diagnosis via serology, biopsy

70
Q

How do you treat Membranous Nephropathy?

A

Supportive

+/- immunosuppressive agents

Transplant (can be recurrent even with a transplant though)

Prognosis depends on renal function and amount of proteinuria. Adverse risk factors for male sex, older age

71
Q

One of the most common causes of PRIMARY glomerular diseases in adults

A

Focal Segmental Glomerulosclerosis (FSGS)

A HISTOLOGIC LESION rather than a specific disease entity) accounting for 35% of all cases of idiopathic nephrotic syndrome in adults

> 70% present with nephrotic syndrome

72
Q

Who is at higher risk for FSGS?

A

African American patients

3-4x more common in men

Typically observed in those aged 18-45 years, although no age group is exempt

73
Q

What is the pathogenesis of FSGS?

A

Glomerular injury resulting from damage to podocytes

Sclerosis in parts (segmental) of at least one glomerulus (focal)

Less than 50% of glomeruli affected

Secondary FSGS can be due to obesity, infection, inflammations, toxins, healed previous glomerular injury, reflex nephropathy

74
Q

How is FSGS treated?

A

Supportive
Immunosuppressive agents if primary FSGS
Disease-specific Treatment if secondary

75
Q

What can indicate a poor prognosis for FSGS?

A

Nephrotic-range proteinuria
African American race
Renal insufficiency

76
Q

Most common cause of ESRD in the US

A

Diabetic Nephropathy

Defined by characteristic structural and functional changes

RETINOPATHY is common - nearly universal in T1DM with nephropathy

77
Q

Peak incidence is usually found in persons who have had DM for …

A

10-20 years

May be present at the time of diagnosis in T2DM

78
Q

What is the pathogenesis of diabetic nephropathy

A

Direct effects of HTN and metabolic abnormalities (hyperglycemia, dyslipidemia)

Morphologic changes appear in the kidney results in increased filtration of serum proteins into the urine

Hyper filtration —> albuminuria —> slowly progressive decline in GFR

79
Q

How do you treat diabetic nephropathy?

A

STRICT GLYCEMIC and BP CONTROL

ACE/ARBs

Statin therapy (or statin plus ezetimibe)

Dialysis and transplant when indicated

80
Q

Deposition of amyloid in the glomerulus leading to proteinuria, reduced GFR, and nephrotic syndrome

A

Renal Amyloidosis

AL amyloidosis (previously Primary Amyloidosis) - monoclonal light chain

AA amyloidosis (previously Secondary Amyloidosis) - chronic inflammatory disease (RA) or infection

81
Q

How do you screen for renal amyloidosis?

A

Serum and urine protein electrophoresis (SPEP and UPEP)

Looking for monoclonal light chain spikes

Prognosis varies depending on the nature, number, and extent of organ involvement

Treatment = referral to nephrology and treat underlying cause