Bacterial Endocarditis and Associated Kidney Disease

There is very strong association between bacterial endocarditis or heart valve infection and kidney disease. Prior to the discovery, development and active use of antibiotics, the majority of the patients developed renal disease (kidney disease) as a consequence of subacute valvular infection. The incidence of clinical renal involvement has dropped significantly with the introduction of effective treatment of bacterial endocarditis with antibiotics. The assessment of renal involvement in bacterial endocarditis is quite difficult as transient changes in urine sediment are generally observed. There may be focal and segmental lesions with normal creatinine clearance. Intravenous drug users are at greater risk of developing bacterial endocarditis.

Staphylococcus aureus infection as the cause of bacterial endocarditis has been reported in majority of the cases that lead to a higher frequency of diffuse glomerular disease. The renal lesions associated with endocarditis involved embolization and infection. The renal lesions could also have immunological basis as immune complex deposits within glomeruli have been detected in majority of the cases. The involvement of complement (an immune response modulator protein in our blood) system during active disease (bacterial endocarditis) in association with immune complexes complicates the severity of intra-glomerular lesions. The two major categories of renal lesions found in patients affected by bacterial endocarditis are: (1) Focal segmental abnormality due to subacute infection and (2) Diffuse glomerular lesions in the patients with acute bacterial endocarditis mimicking the pattern of post-streptococcal glomerulonephritis. The electron micrograph (Fig-1) from the kidney biopsy of a patient with acute glomerulonephritis and acute bacterial endocarditis illustrates the subepithelial immune complex deposits.

Fig-1: Electron micrograph illustrating the hump shaped subepithelial immune complex deposits (D) alongside the glomerular basement membrane (GBM) and urinary space (US), during acute glomerulonephritis. Uranyl acetate and Lead citrate stain.

The assessment of renal involvement in endocarditis may be difficult diagnostic entity as only minor and transient changes are observed in urinary deposit with variable changes in blood biochemistry. The clinician must recognize the status of impaired cardiac output in the first stage and later workout the potential risk of treatment associated antibiotic nephrotoxicity. The assessment of renal function at the time of presentation of case could be helpful to rule out endocarditis associate renal disease or treatment associated antibiotic nephrotoxicity.

Albumin & Casts in Urine and Associated Renal Lesions

Urine analysis is the cheapest and routine investigation which could be of great help to the clinician to reach at a diagnosis of a complex renal disorder. Albuminuria (excretion of albumin in urine) detected on heat test of the urine and the casts detected on microscopic examination of first morning specimen of urine reveal a lot about the associated renal lesions (pathological changes in kidney). Albuminuria we know definitely to be glomerular origin, although the tubules may also play their part in its production. It seems probable that this is mainly due to the glomerular basement membrane (GBM) which separates the epithelium of the tuft from the endothelium lining the capillaries, with increase of its permeability.

Casts are the microscopic accumulations of cells or coagulated proteins or lipids. Casts if present could be detected on microscopic examination of deposit obtained after centrifugation of urine. The casts must also be traced to the glomerulus, at least the essential hyaline matrix of the cast composed of coagulated albumin. Again the tubules add their contribution in the shape of epithelial cells and fatty and granular detritus which give to the casts their characteristic appearance. Careful examination casts is as informative as blood biochemistry investigations in cases of kidney disease. The cast gives a picture of the degenerative changes in the tubules. A hyaline cast indicates slight glomerular leakage without active tubular degeneration. Cellular casts denote marked activity of the morbid process. Granular casts denote moderate activity. The admixture of red blood cells (RBCs) is a sign of glomerular hemorrhage. We find that the study of casts is of remarkable importance in assessing the prognosis of a renal disorder. As long as there is considerable activity there is a scope for improvement. For such a study to be of value, the urine should be fresh. If the urine is alkaline or has been allowed to stand for long time, the casts may largely disappear. The absence of casts in an alkaline urine has not the same significance as when the urine is acidic. The acidity of the urine assists in the formation of casts. Deposition of casts in the tubules may lead to oliguria (low output of urine) leading to edema.

Reversible Renal Failure

When we come across the term reversible renal failure, it indicates that there was a scope for the repair of renal lesions or complete recovery of renal function. Reversible renal failure is of great importance for the clinician/nephrologist attending to the patient, because he/she could be able to do something for the well being of the patient. Clinical end picture may be same in many renal disorders though the origins are so different. Acute stage is characterized by pain in back, fever and edema, a rise in blood pressure and such urinary changes as oliguria (low output of urine), high specific gravity of urine with high coloration. Presence of albumin, red blood cells (RBCs) and casts have also been observed in urine with low urea content. It has been observed that reversible renal failure is generally extra-glomerular in origin, but it may be nephritic type. Most of the cases with acute glomerulonephritis also make a complete recovery with therapy and dialysis.  Tubular damage may also be repaired, as has been in the cases of mercuric chloride poisoning. Accumulation of nitrogenous waste products in blood is observed in these patients without any renal lesion on blood biochemistry and kidney biopsy evaluation. The condition may also be termed as extra-renal uremia or azotemia without corresponding renal lesion.