Penyakit ginjal kronik

- gangguan fungsi ginjal yang menahun bersifat progresif dan irreversibel. Dimana

kemampuan tubuh gagal untuk mempertahankan metabolisme dan keseimbangan

cairan dan elektrolit serta menyebabkan uremia (retensi urea dan sampah nitrogen lain

dalam darah)

- suatu keadaan klinis yang ditandai dengan penurunan fungsi ginjal yang bisa dilihat

dari penurunan GFR yaitu < 60 mL/min/1.73 m2 atau adanya bukti dari kerusakan

ginjal termasuk albuminuria persisten yaitu > 30 mg albumin urin per creatinine urin.1

- The term chronic renal failure applies to the process of continuing significant irreversible reduction in nephron number and typically corresponds to CKD stages 3–5. The pathophysiologic processes and adaptations associated with chronic renal failure will be the focus of this chapter. The dispiriting term end-stage renal disease represents a stage of CKD where the accumulation of toxins, fluid, and electrolytes normally excreted by the kidneys results in the uremic syndrome. This syndrome leads to death unless the toxins are removed by renal replacement therapy, using dialysis or kidney transplantation. These latter interventions are discussed in Chaps. 281 and 282. End-stage renal disease will be supplanted in this chapter by the term stage 5 CKD. (horison)

-

Chronic Kidney Disease (Mc Graw Hill Current diagnosis)

Essentials of Diagnosis

Progressive azotemia over months to years. Symptoms and signs of uremia when nearing end-stage disease.

Hypertension in the majority.

Isosthenuria and broad casts in urinary sediment are common.

Bilateral small kidneys on ultrasound are diagnostic.

Table 22–5. Stages of chronic kidney disease: a clinical action plan.1,2

Stage Description GFR (mL/min/1.73 m2)

Action3

 

 

1 Kidney damage with

normal or GFR90

Diagnosis and treatment. Treatment of comorbid conditions. Slowing of progression. Cardiovascular disease risk reduction.

2 Kidney damage with

mildly GFR

60–89 Estimating progression.

3Moderately GFR

30–59 Evaluating and treating complications.

4Severely GFR

15–29 Preparation for kidney replacement therapy.

5 Kidney failure < 15 (or dialysis) Replacement (if uremia is present).

Table 22–6. Major causes of chronic kidney disease.

Glomerulopathies 

  Primary glomerular diseases: 

    Focal and segmental glomerulosclerosis

    Membranoproliferative glomerulonephritis

    IgA nephropathy

    Membranous nephropathy

  Secondary glomerular diseases: 

    Diabetic nephropathy

    Amyloidosis

    Postinfectious glomerulonephritis

    HIV-associated nephropathy

    Collagen-vascular diseases

    Sickle cell nephropathy

    HIV-associated membranoproliferative glomerulonephritis

Tubulointerstitial nephritis 

  Drug hypersensitivity

  Heavy metals

  Analgesic nephropathy

  Reflux/chronic pyelonephritis

  Idiopathic

Hereditary diseases 

  Polycystic kidney disease

  Medullary cystic disease

  Alport syndrome

Obstructive nephropathies 

  Prostatic disease

  Nephrolithiasis

  Retroperitoneal fibrosis/tumor

  Congenital

Vascular diseases 

  Hypertensive nephrosclerosis

  Renal artery stenosis

Sedangkan Perhimpunan Nefrologi Indonesia (PERNEFRI) tahun 2000 mencatat penyebab

penyakit ginjal kronik yang menjalani hemodialisis di Indonesia yaitu1,4:

1. Glomerulonefritis (46,39%)

2. Diabetes Melitus (18,65%)

3. Obstruksi dan Infeksi (12,85%)

4. Hipertensi (8,46%)

5. Penyakit yang tidak diketahui (13,65%).

Penyebab penyakit ginjal kronik cukup banyak tetapi untuk keperluan klinis dapat dibagi

dalam 2 kelompok : 3,4

1. Penyakit parenkim ginjal

Penyakit ginjal primer : glomerulonefritis, myelonefritis, ginjal polikistik, tbc ginjal

Penyakit ginjal sekunder : nefritis lupus, nefropati, amilordosis ginjal, poliarteritis

nodasa, sclerosis sistemik progresif, gout dan diabetes melitus

2. Penyakit ginjal obstruktif (pembesaran prostat, batu saluran kemih, refluks ureter)

Table 22–7. Symptoms and signs of uremia.

Organ System Symptoms Signs

General Fatigue, weakness Sallow-appearing, chronically ill

Skin Pruritus, easy bruisability Pallor, ecchymoses, excoriations, edema, xerosis

ENT Metallic taste in mouth, epistaxis Urinous breath

Eye   Pale conjunctiva

Pulmonary Shortness of breath Rales, pleural effusion

Cardiovascular Dyspnea on exertion, retrosternal pain on inspiration (pericarditis)

Hypertension, cardiomegaly, friction rub

Gastrointestinal Anorexia, nausea, vomiting, hiccups  

Genitourinary Nocturia, impotence Isosthenuria

Neuromuscular Restless legs, numbness and cramps in legs

 

Neurologic Generalized irritability and inability to concentrate, decreased libido

Stupor, asterixis, myoclonus, peripheral neuropathy

On physical examination, the patient appears chronically ill. Hypertension is common. The skin may be yellow, with signs of easy bruisability. Rarely seen in the dialysis era is uremic frost, a cutaneous reflection of ESRD. Uremic fetor is the characteristic fishy odor of the breath. Cardiopulmonary signs may include rales, cardiomegaly, edema, and a pericardial friction rub. Mental status can vary from decreased concentration to confusion, stupor, and coma. Myoclonus and asterixis are additional signs of uremic effects on the central nervous system.

The term "uremia" is used for this clinical syndrome, but the exact cause remains unknown. BUN and serum creatinine are considered markers for unknown toxins.

In any patient with renal failure, it is important to identify and correct all possibly reversible causes. Urinary tract infections, obstruction, extracellular fluid volume depletion, nephrotoxins, hypertension, and congestive heart failure should be excluded (Table 22–8). Any of the above can worsen underlying chronic renal failure

Imaging

The finding of small echogenic kidneys bilaterally (< 10 cm) by ultrasonography supports a diagnosis of chronic kidney disease, though normal or even large kidneys can be seen with chronic renal failure caused by adult polycystic kidney disease, diabetic nephropathy, HIV-associated nephropathy, multiple myeloma, amyloidosis, and obstructive uropathy. Radiologic evidence of renal osteodystrophy is another helpful finding, since radiographic

changes of secondary hyperparathyroidism do not appear unless parathyroid levels have been elevated for at least 1 year. Evidence of subperiosteal reabsorption along the radial sides of the digital bones of the hand confirms hyperparathyroidism.