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 225. Stages of chronic kidney disease: a clinical action plan.1,2

Stage Description

GFR
(mL/min/1.73
m2)

Kidney damage with

normal or

4
5

GFR

Kidney damage with 6089

mildly

90

Action3

Diagnosis and treatment. Treatment of

comorbid conditions. Slowing of progression.
Cardiovascular disease risk reduction.
Estimating progression.

GFR

Moderately
GFR
Severely

GFR

Kidney failure

3059

Evaluating and treating complications.

1529

Preparation for kidney replacement therapy.

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

Table 226. 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 yaitu 1,4:
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 227. 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
Pulmonary

Pale conjunctiva
Shortness of breath

Rales, pleural effusion

Cardiovascular Dyspnea on exertion, retrosternal pain on Hypertension, cardiomegaly,

inspiration (pericarditis)
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 228).
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, HIVassociated 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.