A 65-Year-Old Man With Hypertension and Proteinuria

Pradeep Arora, MD; Karen Convay, NP


October 12, 2015

Clinical characteristics that predict a faster decline in glomerular filtration rate include greater proteinuria, higher blood pressure, black ethnicity, a lower serum high-density lipoprotein cholesterol level, and a lower serum transferrin level. In this patient, the rate of progression was very fast. Factors that led to faster progression of CKD here included uncontrolled blood pressure, diabetes, nephrotic-range proteinuria, and black ethnicity.[1]The ideal blood pressure goal in patients such as this is < 130/80 mm Hg.

Renin-angiotensin system (RAS) blockers are the first choice for treatment, along with sodium restriction and diuretics in patients with proteinuria. However, data on use of RAS blockers in elderly patients with CKD who are nondiabetic and nonproteinuric are lacking. Other measures to slow progression of kidney disease include a low-protein diet, better control of blood sugar, control of proteinuria (goal, < 0.5 g/day), smoking cessation, and lipid control.[2,3]

Anemia is a common complication in patients with CKD. The most important cause of anemia is lack of production of erythropoietin by interstitial cells in the kidney. Other causes include decreased RBC survival, bleeding diathesis, iron deficiency, chronic inflammation, and folate deficiency. Treatment includes use of recombinant erythropoietin after replenishing iron to a saturation > 20%.

Renal bone disease is a common complication of CKD. It is defined as an abnormality of calcium, phosphorus, parathyroid hormone (PTH), or vitamin D metabolism; an abnormality in bone turnover, mineralization, volume linear growth, or strength; or extraskeletal calcification.

Different types of bone disease occur in CKD; these include:

  • High-turnover bone disease from high PTH levels

  • Low-turnover bone disease (adynamic bone disease)

  • Defective mineralization (osteomalacia)

  • Mixed disease

  • Beta-2-microglobulin–associated bone disease

Factors associated with secondary hyperparathyroidism include hyperphosphatemia; hypocalcemia; decreased renal synthesis of 1,25-dihydroxycholecalciferol (1,25-dihydroxyvitamin D, or calcitriol); an intrinsic alteration of the parathyroid glands, which gives rise to increased PTH secretion; and increased parathyroid growth and skeletal resistance to PTH.

Treatment of secondary hyperparathyroidism includes correction of serum phosphorus and calcium levels. Vitamin D and calcimimetics are used to treat secondary hyperparathyroidism.


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