Bài giảng bệnh cầu thận và các hội chứng lâm sàng

Bệnh cầu thận và các hội chứng lâm sàng... Renal Pathology Outline• Bệnh lý cầu thận: Viêm cầu thận – Glomerular diseases: Glomerulonephritis • Bệnh lý ống thận: hoại tử ống thận cấp – T

Bệnh cầu thận và các hội chứng lâm sàng

• 150gm: each kidney

• 1700 liters of blood filtered  180 L of G filtrate  1.5 L of urine / day

• Kidney is a retro-peritoneal organ

• Blood supply: Renal Artery & Vein

• One half of kidney is sufficient – reserve

• Kidney function: Filtration, Excretion, Secretion,

Hormone synthesis

Collecting Duct

peritubular capillaries

Cấu trúc cầu thận

Chức năng thận

A Hằng định nội mô

1 Bài tiết nước (urine formation)

a Nitrogenous end products: urea, creatinine, uric acid…

b Metabolic degradation of peptide hormones:

glucagon, insulin, PTH, growth hormone, FSH, and gastrin.

2 Cân bằng dịch/điện giải (Na+, K+, water,

Ca++, Mg++, Phosphate PO 4 3-)

3 Điều hòa Acid/base:

• kidneys generate and reclaim filtered bicarbonate,

as well as secrete excess acid to maintain balance

B Các chức năng khác

1 Bài tiết Renin-angiotensin kiểm soát huyết áp

a Thận rất nhạy với tình trạng giảm HA

– Kidney senses decreased BP

b Tiết renin: chuyển AG I thành AG II

– Secretes renin (enzyme), which converts Angiotensin I to angiotensin II

c AG II co mạch: tăng HA

– Angiotensin II is a vasoconstrictor  increased BP

d AG II kích thích tiết aldosterone

– Angiotensin II also stimulates aldosterone secretion

e Aldosterone tăng tái hấp thu Na, nước

– Aldosterone increases Na+ and H2O reabsorption, increased plasma volume, and increased BP (aldosterone also stimulates potassium secretion into tubules)

c  RBC formation is mainly due to 

erythropoietin production in the

diseased kidneys,

3 Duy trì nội mô Calcium-Phosphorus bone

a Activates Vitamin D (Hydroxylation of 25-OH-D3

to 1,25-OH-D3) in kidney disease, can supplement calcitriol, but very expensive Low vit D  less Ca++ absorbed

b Inverse relationship between Ca++ and P, so

when P is retained by diseased kidney, Ca++ levels decline (less calcium reabsorbed by the kidney).

c Low serum calcium  parathyroid gland releases

PTH: Parathyroid Hormone: works to elevate serum Ca++ by pulling it from the bones  fragility, muscular weakness, decreased

muscular tone, and general neuromuscular hypoexcitability

• Azotemia:  BUN, creatinine

• Uremia: azotemia + more problems

• Acute renal failure: oliguria

• Chronic renal failure: prolonged uremia

Abnormal findings

Renal Pathology Outline

• Bệnh lý cầu thận: Viêm cầu thận

– Glomerular diseases: Glomerulonephritis

• Bệnh lý ống thận: hoại tử ống thận cấp

– Tubular diseases: Acute tubular necrosis

• Bệnh thận kẽ: viêm thận bể thận

– interstitial diseases: Pyelonephritis

• Bệnh mạch máu thận: xơ hóa thận

– Diseases involving blood vessels: Nephrosclerosis

• Nang thận

– Cystic diseases

• Tumors

Clinical Syndromes:

• Nephritic syndrome-hội chứng thận viêm

– Thiểu niệu, tiểu máu, protein niệu, phù

• Nephrotic syndrome-hội chứng thận hư

– Protein niệu đại lượng, giảm albumin máu, tăng lipid máu, phù

• Acute renal failure –suy thận cấp

– Thiểu niệu, mất chức năng thận trong vài tuần

• Chronic renal failure-suy thận mạn

– Mất dần chức năng thận > 3 tháng, hội chứng ure máu cao

Cơ chế phù trong bệnh lý cầu thận

A Hội chứng thận hư:

1 Protein niệu-Proteinuria

(hallmark of nephrotic syndrome) – urinary protein loss of >3g/day

(2’ increased capillary permeability)

a Giảm albumin máu-Hypoalbuminemia

b Mất IG-loss of immunoglobulins

c Mất transferin-loss of transferrin

d Mất protein tải VitD-loss of vitamin D

binding protein

2 Phù-Edema 2’

3 Tăng lipid máu-Hyperlipidemia

4 Also possible:

o rối loạn đông máu, tăng đông

• blood coagulation disorders or increased

clotting (can  occlusions in lungs and legs)

I Hội chứng thận viêm-Nephritic

Syndrome: group of diseases characterized by

glomerular inflammation (glomerulonephritis)

• Hematuria, HTN, mild  in renal fx.

• Caused by infection, SLE, other causes

• Acute: either resolves or  nephrotic syndrome or

ESRD.

• MNT: maintain good nutr Status

• (no restriction of prot/K+)

• If HTN, restrict Na+

Viêm cầu thận

Các nguyên nhân của bệnh lý cầu thận- Glomerular diseases

– Nephrotic syndrome

• Minimal change disease

• Focal segmental glomerulosclerosis

• Tubular and interstitial diseases

– Inflammatory lesions

• pyelonephritis

Bệnh lý ống thận và thận kẽ

• Invasive kidney infection

• Usually ascends from UTI

• Fever, flank pain

• Organisms: E coli , Proteus

• Women, elderly

• Patients with catheters or mal-formations

• Dysuria, frequency

• Organisms: E coli, Proteus

Urinary Tract Infection

Drug-Induced Interstitial Nephritis

• Antibiotics, NSAIDS

• IgE and T-cell-mediated immune reaction

• Fever, eosinophilia, hematuria

• Patient usually recovers

• Analgesic nephritis is different (bad)

Acute Tubular Necrosis

• The most common cause of ARF!

• Reversible tubular injury

• Many causes: ischemic (shock), toxic (drugs)

• Most patients recover

III Acute Renal Failure (ARF):

Sudden drop in GFR Can develop in a

previously healthy person, and last from a few days to several weeks

A Causes

1 Prerenal: sudden drop in blood volume

or renal bloodflow due to severe dehydration, shock or trauma.

2 Intrinsic : damage to kidney cells 2’

sustained shock, trauma, surgery, septicemia, nephrotoxic agents, acute glomerulonephritis.

3 Postrenal: (obstructive) Kidneys can

form urine, but excretion is impeded.

feeling, n/v/d, itching (pruritis 2’ Ca,

Na deposition), muscle cramps,

hiccups, twitching, emotional irritability,  mental capacity

2 Proteinuria

3 Hyperkalemia (2’  clearance;

nephropathy can cause deficiency in or resistance to aldosterone)

4 Sodium: sodium retention resulting in

fluid retention, HTN, edema, CHF

– Some patients experience loss of high

amounts of sodium: salt losing

enteropathy

5 Hyperphosphatemia

6 Acid-base balance:  uric acid secretion

and bicarbonate production 

metabolic acidosis

7 Blood volume changes

a Oliguric phase: very little urinary output – blood pressure rises

sharply Can  pulmonary edema (remember from HTN chapter)

b Diuretic phase: large losses of

fluids and electrolytes

c Recovery phase: (hopefully) –

everything normalizes

Xơ hóa cầu thtận lành tính Benign Nephrosclerosis

• Found in patients with benign hypertension

• Hyaline thickening of arterial walls

• Leads to mild functional impairment

• Rarely fatal

Benign nephrosclerosis

Xơ hóa cầu thận ác tính

• 5% of cases of hypertension

• Super-high blood pressure, encephalopathy, heart abnormalities

• First sign often headache, scotomas

• Decreased blood flow to kidney leads to increased renin, which leads to increased BP!

• 5y survival: 50%

Tăng huyết áp ác tính

Malignant Hypertension

Bệnh thận đa nang

Adult Polycystic Kidney Disease

• Autosomal dominant

• Huge kidneys full of cysts

• Usually no symptoms until 30 years

• Associated with brain aneurysms.

Adult polycystic kidney disease

Childhood Polycystic Kidney Disease

• Autosomal recessive

• Numerous small cortical cysts

• Associated with liver cysts

• Patients often die in infancy

Childhood polycystic kidney disease

Medullary Cystic Kidney Disease

• Chronic renal failure in children

• Complex inheritance

• Kidneys contracted, with many cysts

• Progresses to end-stage renal disease

Renal Cell Carcinoma

Renal cell carcinoma

Bladder Carcinoma

• Derived from transitional epithelium

• Present with painless hematuria

• Prognosis depends on grade and depth of invasion

• Overall 5y survival = 50%

Bladder carcinoma

Bệnh thận mạn

Chronic Kidney Disease (CKD, previouslyCRF)

Irreversible, progressive destruction of nephrons Leads to End Stage Renal

Disease (ESRD)

A Causes

1 ARF

2 Nephritis, renal artery obstruction,

kidney stones, nephrotic syndrome, polycystic kidney disease

3 Diabetic nephropathy

4 HTN, atherosclerosis

www.kidney.org

B Progression

1 Magnification Phenomenon: As GFR falls, 

function of remaining nephrons (adaptive hypertrophy)

This is why it can go undetected At Stage I: Protein restriction and conservative

management can slow progression to ESRD Control HTH and DM

2 Kidney damage with normal or  GFR

a  renal reserve, but asymptomatic

b BUN, lytes,fluid balance, P, Ca++ ALL

NORMAL

3 Renal Insufficiency

a Mild azotemia (mildly increased BUN,

creat)

b Impaired concentration of urine: urine

output is probably OK at this point, but

because concentrating ability is impaired,

we see nocturia

c Mild anemia

d Fatigue and decreased mental acuity

e Challenges will accelerate renal

deterioration (ie excessive protein load, P load, or uncontrolled HTN, DM, etc.)

4 Frank Renal Failure

a Anemia (normochromic normocytic, but low Hgb/Hct)

b Uremia

c Poss GI ulceration and bleeding

d Skin: may become yellowed Urea

from sweat may crystallize on skin = uremic frost Pruritis (itching)

e PEM 

f HTN

5 ESRD End-Stage Renal Disease: GFR <20%