**5.1 Clinical manifestation and management**

What is the best way to manage these individuals? In the outpatient setting, achecklist for each patient ensures that each individual's needs are met. A list of "ten commandments" for the CKD patient is:


Treat hyperurricemia with allopurinol if the eGFR is >30 ml/min.

8. Phosphate binders, precursor vitamin D and active D (when necessary). We are using both calcium and non-calcium containing binders in our clinic. We try to keep serum calcium levels less than or equal to 9.5 mg%. Vitamin D2 and 3 are used in patients with 25(OH)D levels less than 30 ng/ml. Active vitamin D is used to control elevated iPTH levels and the effects of secondary HPT.


Diabetic patients should maintain euglycemia, insulin requirements may decrease as CKD progresses. Metformin should be avoided and glipizide isthe preferred oral agentbecause it is not downgraded to a metabolite excreted by the kidneys.

#### **6. Summary**

22 Chronic Kidney Disease

(compensatory hypertrophy). This leads to hemodynamic changes including glomerular hypertension and hyperfiltration. There is reduced afferent arteriolar resistance and intraglomerular pressure rises with increased filtration by the remaining nephrons. The intrinsic and extrinsic cells contribute to sclerosis as mentioned above contributing to the

Tubulointerstitial injury results from ischemia of tubule segments downstream from sclerotic glomeruli. Acute and chronic inflammation in the adjacent interstitium, and damage of pericapillary blood supply also contribute to tubular injury. The above events

Angiotensin II increases vascular tone (predominantly post-glomerular) and affects intraglomerular pressure. The increased pressure alters the structure of the pores in the

What is the best way to manage these individuals? In the outpatient setting, achecklist for each patient ensures that each individual's needs are met. A list of "ten commandments" for

2. Round up the usual suspects. Diabetes and hypertension account for almost ¾ of the patient population. Urinalysis, serologies, sonography and biopsy (if necessary) to

3. Fix what you can. Discontinue NSAIDs, correct volume depletion and treat BPH (men)

5. Measure (spot urine protein /creatinine) and treat proteinuria. The goal is<300mg/day. Maximize the dose of an ACE inhibitor, then add an ARB at ½ full dose and increase to reach goal. Loop diuretics are essential to manage edema fluid and offset the development of hyperkalemia. Renin blockers and aldosterone antagonists are added with monitoring of the patient's potassium and creatinine. If the potassium rises to greater than 5.5 meq/l or if the serum creatinine increases more than 30% above

6. Treat anemia of CKD with an ESA if there is no blood loss and iron stores are adequate. Check thyroid function, B-12, folic acid levels. The target Hgb is >10g/dl. Parenteral

7. Give base supplements to correct metabolic acidosis. Untreated acidosis causes osteopenia and muscle catabolism, along with the release of calcium and phosphorous

8. Phosphate binders, precursor vitamin D and active D (when necessary). We are using both calcium and non-calcium containing binders in our clinic. We try to keep serum calcium levels less than or equal to 9.5 mg%. Vitamin D2 and 3 are used in patients with 25(OH)D levels less than 30 ng/ml. Active vitamin D is used to control elevated iPTH

from bone. Sodium bicarbonate is replaced at 0.5-1.0 meq/kg/day. Treat hyperurricemia with allopurinol if the eGFR is >30 ml/min.

Use ACE, ARB, both, renin blockers, calcium channel blockers, aldosterone antagonists,

along with proteinuria eventually lead to tubulointerstitial fibrosis.

glomerular basement membrane (GBM) and increases proteinuria.

focal and segmental glomerulosclerosis.

**5.1 Clinical manifestation and management** 

1. Estimate the GFR and stage the patient's CKD.

4. Treat hypertension. Goal of therapy is <130/80.

baseline, dosages will need to be decreased.

iron may be needed to keep the TSAT > 25%.

levels and the effects of secondary HPT.

and bladder dysfunction (women).

the CKD patient is:

make the diagnosis.

loop diuretics as needed.

CKD will remain a health concern into the future. CKD clinics managing patients in a coordinated fashion with nutritionists and surgeons will improve lives. Better blood pressure control with diminution of proteinuria will slow the progress of established disease. Attention to acidemia and hyperruricemia will also be beneficial. New insights into the pathogenesis and treatment of diabetes may help manage the number one cause of kidney failure in America.

#### **7. References**


**3**

*1,2Republic of Macedonia* 

*3Japan* 

**The New Kidney and Bone Disease:**

Igor G. Nikolov1, Ognen Ivanovski2 and Nobuhiko Joki3

*3Division of Nephrology, Toho University Ohashi Medical Center, Tokyo,* 

Kidney is one of the most important organs in the regulation of mineral metabolism (Fukagawa et al., 2006). Chronic kidney disease (CKD) is a worldwide public health problem that affects 5% to 10% of the world population, with increasing prevalence and adverse outcomes, including progressive loss of kidney function, cardiovascular disease, and premature death (Eknoyan et al., 2004). Calcium and phosphorus are fundamentally important in a wide array of biological functions. Abnormalities in calcium, phosphorus, parathyroid hormone (PTH), and vitamin D metabolism (usually referred to as disordered mineral metabolism) are common in patients with (CKD) (Block et al., 1998). Cardiovascular disease is the leading cause of death in patients with CKD (London et al., 2003). It has been shown that in individuals with kidney failure on maintenance dialysis who are younger than 65 years, cardiovascular mortality is 10 to 500 times higher than in the general population, even after adjustment for sex, race, and presence of diabetes (Foley RN et al., 1998). Disturbances in mineral metabolism are common complications of CKD and an important cause of morbidity and decreased quality of life. Importantly, increasing evidence suggests that these disturbances are associated with changes in arterial compliance, cardiovascular calcification, bone disorders and all-cause and cardiovascular mortality (Palmer SC et al., 2005, Drueke et al., 2010). Traditionally, when defining bone diseases in CKD patients, this group of disorders has been usually termed renal osteodystrophy. However, beside strictly defined, the term renal osteodystrophy means only bone abnormalities. Recently, the KDIGO (Kidney Disease: Improving Global Outcomes) conference group agreed that the definition of renal osteodystrophy should be only specific to bone pathology found in patients with CKD (Moe S. et al., 2006). It has been concluded that renal osteodystrophy is one component of the mineral and bone disorders that occur as a complication of CKD. It has been proposed that the evaluation and definitive diagnosis of renal osteodystrophy requires performing a bone biopsy. Histomorphometry is not essential for clinical diagnosis, but should be performed in research studies. There was an agreement that histomorphometric results are to be reported by use of the standard nomenclature

**1. Introduction** 

**Chronic Kidney Disease – Mineral** 

**and Bone Disorder (CKD–MBD)** 

*1University Clinic of Nephrology, Medical Faculty - Skopje, 2University Clinic of Urology, Medical Faculty - Skopje,* 

