THE UREMIA PATIENT

An introductory account is given of the terms of azotaemia (biochemica l symptom: rise of urea level) and uraemia (clinical symptoms: increas e in N-metabolites, impairment of hoemeostasis). The aetiopathogenetic ally different forms of uraemia are discussed, that is renal, extraren al, acute and chronic processes. Chronic renal insufficiency is quite frequent and is pathophysiologically based on hyperperfusion with wate r and solutes of remaining functional nephrons. It may be subdivided b y five stages according to wasting of nephrons. Polyuria/polydypsia, w ith serum creatinine still normal, was found to occur as the first sym ptom but not until two thirds of all nephrons have been lost. Renal an d extrarenal kidney insufficiency is pathophysiologically characterise d by hypoperfusion due to impaired intrarenal circulation. Therapy of chronic kidney insufficiency is largely of palliative nature, that is no-stress patient keeping with dehydration as well as water and electr olyte substitution. Limitation of protein-phosphorus uptake and, occas ionally, common salt uptake is the essential therapeutic element. Bloo d urea is to be kept below 20 mmol/l (120 mg/dl) by dietary measures, such as 14 to 17 percent of high-quality and highly digestible protein and 0.2 to 0.15 percent of phosphorus in dry weight of feedstuff. Inc reased N-metabolite levels will result in increased circulation and in filtration of remaining nephrons and will thus actually initiate a vi cious circle leading to wasting of additional nephrons and deteriorati on of kidney functions (hyperfiltration theory). If pharmaceuticals wi th renal excretion are administered (chemotherapeutics, cardiac glycos ides), doses and/or application intervals should be reduced or increas ed, depending on severity of the given case of kidney insufficiency. I n oligo-anuric conditions, diuresis should be urgently activated, usin g furosemide or mannitol or hypertonic glucose solutions.